Arquivo da tag: neurociências

Spirituality, Religion May Protect Against Major Depression by Thickening Brain Cortex (Science Daily)

Jan. 16, 2014 — A thickening of the brain cortex associated with regular meditation or other spiritual or religious practice could be the reason those activities guard against depression — particularly in people who are predisposed to the disease, according to new research led by Lisa Miller, professor and director of Clinical Psychology and director of the Spirituality Mind Body Institute at Teachers College, Columbia University.

The study, published online by JAMA Psychiatry, involved 103 adults at either high or low risk of depression, based on family history. The subjects were asked how highly they valued religion or spirituality. Brain MRIs showed thicker cortices in subjects who placed a high importance on religion or spirituality than those who did not. The relatively thicker cortex was found in precisely the same regions of the brain that had otherwise shown thinning in people at high risk for depression.

Although more research is necessary, the results suggest that spirituality or religion may protect against major depression by thickening the brain cortex and counteracting the cortical thinning that would normally occur with major depression. The study, published on Dec. 25, 2013, is the first published investigation on the neuro-correlates of the protective effect of spirituality and religion against depression.

“The new study links this extremely large protective benefit of spirituality or religion to previous studies which identified large expanses of cortical thinning in specific regions of the brain in adult offspring of families at high risk for major depression,” Miller said.

Previous studies by Miller and the team published in theAmerican Journal of Psychiatry (2012) showed a 90 percent decrease in major depression in adults who said they highly valued spirituality or religiosity and whose parents suffered from the disease. While regular attendance at church was not necessary, a strong personal importance placed on spirituality or religion was most protective against major depression in people who were at high familial risk.

Journal Reference:

  1. Lisa Miller, Ravi Bansal, Priya Wickramaratne, Xuejun Hao, Craig E. Tenke, Myrna M. Weissman, Bradley S. Peterson.Neuroanatomical Correlates of Religiosity and SpiritualityJAMA Psychiatry, 2013; : 1 DOI:10.1001/jamapsychiatry.2013.3067

Brain Regions ‘Tune’ Activity to Enable Attention (Science Daily)

Jan. 16, 2014 — The brain appears to synchronize the activity of different brain regions to make it possible for a person to pay attention or concentrate on a task, scientists at Washington University School of Medicine in St. Louis have learned.

 Scientists at the Neuroimaging Laboratory at Washington University School of Medicine in St. Louis have learned that brain regions sync their activity levels to enable attention. Pictured (from left) are first author Amy Daitch, co-senior author Maurizio Corbetta, postdoctoral researcher Alicia Callejas and McDonnell Scholar Lenny Ramsey. (Credit: Robert J. Boston)

Researchers think the process, roughly akin to tuning multiple walkie-talkies to the same frequency, may help establish clear channels for communication between brain areas that detect sensory stimuli.

“We think the brain not only puts regions that facilitate attention on alert but also makes sure those regions have open lines for calling each other,” said first author Amy Daitch, a graduate student researcher.

The results are available in the Proceedings of the National Academy of Sciences.

People who suffer from brain injuries or strokes often have problems paying attention and concentrating.

“Attention deficits in brain injury have been thought of as a loss of the resources needed to concentrate on a task,” said senior author Maurizio Corbetta, MD, the Norman J. Stupp Professor of Neurology. “However, this study shows that temporal alignment of responses in different brain areas is also a very important mechanism that contributes to attention and could be impaired by brain injury.”

Attention lets people ignore irrelevant sensory stimuli, like a driver disregarding a ringing cell phone, and pay attention to important stimuli, like a deer stepping onto the road in front of the car.

To analyze brain changes linked to attention, the scientists used grids of electrodes temporarily implanted onto the brains of patients with epilepsy. Co-senior author Eric Leuthardt, MD, associate professor of neurosurgery and bioengineering, uses the grids to map for surgical removal of brain tissues that contribute to uncontrollable seizures.

With patient permission, the grids also can allow Leuthardt’s lab to study human brain activity at a level of detail unavailable via any other method. Normally, Corbetta and his colleagues investigate attention using various forms of magnetic resonance imaging (MRI), which can detect changes in brain activity that occur every 2 to 3 seconds. But with the grids in place, Corbetta and Leuthardt can study the changes that occur in milliseconds.

Before grid implantation, the scientists scanned the brains of seven epilepsy patients, using MRI to map regions known to contribute to attention. With the grids in place, the researchers monitored brain cells as the patients watched for visual targets, directing their attention to different locations on a computer screen without moving their eyes. When patients saw the targets, they pressed a button to let the scientists know they had seen them.

“We analyzed brain oscillations that reflect fluctuations in excitability of a local brain region; in other words, how difficult or easy it is for a neuron to respond to an input,” Daitch said. “If areas of the brain involved in detecting a stimulus are at maximum excitability, you would be much more likely to notice the stimulus.”

Excitability regularly rises and falls in the cells that make up a given brain region. But these oscillations normally are not aligned between different brain regions.

The researchers’ results showed that as patients directed their attention, the brain regions most important for paying attention to visual stimuli adjusted their excitability cycles, causing them to start hitting the peaks of their cycles at the same time. In regions not involved in attention, the excitability cycles did not change.

“If the cycles of two brain regions are out of alignment, the chances that a signal from one region will get through to another region are reduced,” Corbetta said.

Daitch, Corbetta and Leuthardt are investigating whether knowing not just the location, but also the tempo of the task, allows participants to bring the excitability of their brain regions into alignment more rapidly.

Journal Reference:

  1. A. L. Daitch, M. Sharma, J. L. Roland, S. V. Astafiev, D. T. Bundy, C. M. Gaona, A. Z. Snyder, G. L. Shulman, E. C. Leuthardt, M. Corbetta. Frequency-specific mechanism links human brain networks for spatial attention.Proceedings of the National Academy of Sciences, 2013; 110 (48): 19585 DOI: 10.1073/pnas.1307947110

Discovery of Quantum Vibrations in ‘Microtubules’ Inside Brain Neurons Supports Controversial Theory of Consciousness (Science Daily)

Jan. 16, 2014 — A review and update of a controversial 20-year-old theory of consciousness published in Physics of Life Reviews claims that consciousness derives from deeper level, finer scale activities inside brain neurons. The recent discovery of quantum vibrations in “microtubules” inside brain neurons corroborates this theory, according to review authors Stuart Hameroff and Sir Roger Penrose. They suggest that EEG rhythms (brain waves) also derive from deeper level microtubule vibrations, and that from a practical standpoint, treating brain microtubule vibrations could benefit a host of mental, neurological, and cognitive conditions.

A review and update of a controversial 20-year-old theory of consciousness published in Physics of Life Reviews claims that consciousness derives from deeper level, finer scale activities inside brain neurons. (Credit: © James Steidl / Fotolia)

The theory, called “orchestrated objective reduction” (‘Orch OR’), was first put forward in the mid-1990s by eminent mathematical physicist Sir Roger Penrose, FRS, Mathematical Institute and Wadham College, University of Oxford, and prominent anesthesiologist Stuart Hameroff, MD, Anesthesiology, Psychology and Center for Consciousness Studies, The University of Arizona, Tucson. They suggested that quantum vibrational computations in microtubules were “orchestrated” (“Orch”) by synaptic inputs and memory stored in microtubules, and terminated by Penrose “objective reduction” (‘OR’), hence “Orch OR.” Microtubules are major components of the cell structural skeleton.

Orch OR was harshly criticized from its inception, as the brain was considered too “warm, wet, and noisy” for seemingly delicate quantum processes.. However, evidence has now shown warm quantum coherence in plant photosynthesis, bird brain navigation, our sense of smell, and brain microtubules. The recent discovery of warm temperature quantum vibrations in microtubules inside brain neurons by the research group led by Anirban Bandyopadhyay, PhD, at the National Institute of Material Sciences in Tsukuba, Japan (and now at MIT), corroborates the pair’s theory and suggests that EEG rhythms also derive from deeper level microtubule vibrations. In addition, work from the laboratory of Roderick G. Eckenhoff, MD, at the University of Pennsylvania, suggests that anesthesia, which selectively erases consciousness while sparing non-conscious brain activities, acts via microtubules in brain neurons.

“The origin of consciousness reflects our place in the universe, the nature of our existence. Did consciousness evolve from complex computations among brain neurons, as most scientists assert? Or has consciousness, in some sense, been here all along, as spiritual approaches maintain?” ask Hameroff and Penrose in the current review. “This opens a potential Pandora’s Box, but our theory accommodates both these views, suggesting consciousness derives from quantum vibrations in microtubules, protein polymers inside brain neurons, which both govern neuronal and synaptic function, and connect brain processes to self-organizing processes in the fine scale, ‘proto-conscious’ quantum structure of reality.”

After 20 years of skeptical criticism, “the evidence now clearly supports Orch OR,” continue Hameroff and Penrose. “Our new paper updates the evidence, clarifies Orch OR quantum bits, or “qubits,” as helical pathways in microtubule lattices, rebuts critics, and reviews 20 testable predictions of Orch OR published in 1998 — of these, six are confirmed and none refuted.”

An important new facet of the theory is introduced. Microtubule quantum vibrations (e.g. in megahertz) appear to interfere and produce much slower EEG “beat frequencies.” Despite a century of clinical use, the underlying origins of EEG rhythms have remained a mystery. Clinical trials of brief brain stimulation aimed at microtubule resonances with megahertz mechanical vibrations using transcranial ultrasound have shown reported improvements in mood, and may prove useful against Alzheimer’s disease and brain injury in the future.

Lead author Stuart Hameroff concludes, “Orch OR is the most rigorous, comprehensive and successfully-tested theory of consciousness ever put forth. From a practical standpoint, treating brain microtubule vibrations could benefit a host of mental, neurological, and cognitive conditions.”

The review is accompanied by eight commentaries from outside authorities, including an Australian group of Orch OR arch-skeptics. To all, Hameroff and Penrose respond robustly.

Penrose, Hameroff and Bandyopadhyay will explore their theories during a session on “Microtubules and the Big Consciousness Debate” at the Brainstorm Sessions, a public three-day event at the Brakke Grond in Amsterdam, the Netherlands, January 16-18, 2014. They will engage skeptics in a debate on the nature of consciousness, and Bandyopadhyay and his team will couple microtubule vibrations from active neurons to play Indian musical instruments. “Consciousness depends on anharmonic vibrations of microtubules inside neurons, similar to certain kinds of Indian music, but unlike Western music which is harmonic,” Hameroff explains.

Journal References:

  1. Stuart Hameroff and Roger Penrose. Consciousness in the universe: A review of the ‘Orch OR’ theoryPhysics of Life Reviews, 2013 DOI: 10.1016/j.plrev.2013.08.002
  2. Stuart Hameroff, MD, and Roger Penrose. Reply to criticism of the ‘Orch OR qubit’–‘Orchestrated objective reduction’ is scientifically justifiedPhysics of Life Reviews, 2013 DOI: 10.1016/j.plrev.2013.11.00
  3. Stuart Hameroff, Roger Penrose. Consciousness in the universePhysics of Life Reviews, 2013; DOI:10.1016/j.plrev.2013.08.002

SHY Hypothesis Explains That Sleep Is the Price We Pay for Learning (Science Daily)

Jan. 9, 2014 — Why do animals ranging from fruit flies to humans all need to sleep? After all, sleep disconnects them from their environment, puts them at risk and keeps them from seeking food or mates for large parts of the day.

Sleeping puppy. Is sleep the price the brain must pay for learning and memory? (Credit: © paul prescott / Fotolia)

Two leading sleep scientists from the University of Wisconsin School of Medicine and Public Health say that their synaptic homeostasis hypothesis of sleep or “SHY” challenges the theory that sleep strengthens brain connections. The SHY hypothesis, which takes into account years of evidence from human and animal studies, says that sleep is important because it weakens the connections among brain cells to save energy, avoid cellular stress, and maintain the ability of neurons to respond selectively to stimuli.

“Sleep is the price the brain must pay for learning and memory,” says Dr. Giulio Tononi, of the UW Center for Sleep and Consciousness. “During wake, learning strengthens the synaptic connections throughout the brain, increasing the need for energy and saturating the brain with new information. Sleep allows the brain to reset, helping integrate, newly learned material with consolidated memories, so the brain can begin anew the next day. ”

Tononi and his co-author Dr. Chiara Cirelli, both professors of psychiatry, explain their hypothesis in a review article in today’s issue of the journal Neuron. Their laboratory studies sleep and consciousness in animals ranging from fruit flies to humans; SHY takes into account evidence from molecular, electrophysiological and behavioral studies, as well as from computer simulations. “Synaptic homeostasis” refers to the brain’s ability to maintain a balance in the strength of connections within its nerve cells.

Why would the brain need to reset? Suppose someone spent the waking hours learning a new skill, such as riding a bike. The circuits involved in learning would be greatly strengthened, but the next day the brain will need to pay attention to learning a new task. Thus, those bike-riding circuits would need to be damped down so they don’t interfere with the new day’s learning.

“Sleep helps the brain renormalize synaptic strength based on a comprehensive sampling of its overall knowledge of the environment,” Tononi says, “rather than being biased by the particular inputs of a particular waking day.”

The reason we don’t also forget how to ride a bike after a night’s sleep is because those active circuits are damped down less than those that weren’t actively involved in learning. Indeed, there is evidence that sleep enhances important features of memory, including acquisition, consolidation, gist extraction, integration and “smart forgetting,” which allows the brain to rid itself of the inevitable accumulation of unimportant details. However, one common belief is that sleep helps memory by further strengthening the neural circuits during learning while awake. But Tononi and Cirelli believe that consolidation and integration of memories, as well as the restoration of the ability to learn, all come from the ability of sleep to decrease synaptic strength and enhance signal-to-noise ratios.

While the review finds testable evidence for the SHY hypothesis, it also points to open issues. One question is whether the brain could achieve synaptic homeostasis during wake, by having only some circuits engaged, and the rest off-line and thus resetting themselves. Other areas for future research include the specific function of REM sleep (when most dreaming occurs) and the possibly crucial role of sleep during development, a time of intense learning and massive remodeling of brain.

This work was supported by NIMH (1R01MH091326 and 1R01MH099231 to GT and CC)

Journal Reference:

  1. Giulio Tononi, Chiara Cirelli. Sleep and the Price of Plasticity: From Synaptic and Cellular Homeostasis to Memory Consolidation and IntegrationNeuron, 2014; 81 (1): 12 DOI: 10.1016/j.neuron.2013.12.025

A mulher que encolheu o cérebro humano (O Globo)

Suzana Herculano é a primeira brasileira a falar na prestigiada conferência TED

Ela debaterá o cérebro de 86 bilhões de neurônios (e não 100 bilhões, como se acreditava) e como o homem se diferenciou dos primatas 

Publicado:24/05/13 – 7h00; Atualizado:24/05/13 – 11h41

Suzana Herculano-Houzel, professora do Instituto de Ciências Biomédicas da UFRJFoto: Guito Moreto

Suzana Herculano-Houzel, professora do Instituto de Ciências Biomédicas da UFRJ Guito Moreto

Neurocientista da UFRJ, Suzana Herculano-Houzel é a primeira brasileira a participar da TED (Tecnologia, Entretenimento e Design, em português) — prestigiada série de conferências que reúne grandes nomes das mais diversas áreas do conhecimento para debater novas ideias. Suzana falará no dia 12 de junho, sob o tema “Ouça a natureza”, e destacará suas descobertas únicas sobre o cérebro humano.

Sobre o que vai falar na TED?

Vou falar sobre o cérebro humano e mostrar como ele não é um cérebro especial, uma exceção à regra. Nossas pesquisas nos revelaram que se trata apenas de um cérebro de primata grande. O notável é que passamos a ter um cérebro enorme, do tamanho que nenhum outro primata tem, nem os maiores, porque inventamos o cozimento dos alimentos e, com isso, passamos a ter um número enorme de neurônios.

O cozimento foi fundamental para nos tornarmos humanos?

Sim, burlamos a limitação energética imposta pela dieta crua. E a implicação bacana e irônica é que, com isso, conseguimos liberar tempo no cérebro para nos dedicarmos a outras coisas (que não buscar alimentos), como criar a agricultura, as civilizações, a geladeira e a eletricidade. Até o ponto em que conseguir comida cozida e calorias em excesso ficou tão fácil que, agora, temos o problema inverso: estamos comendo demais. Por isso, voltamos à saladinha.

Se alimentarmos orangotangos e gorilas com comida cozida eles serão tão inteligentes quanto nós?

Sim, porque não seriam limitados pelo número reduzido de calorias que conseguem com a comida crua. Claro que nós fizemos uma inovação cultural ao inventar a cozinha. Tem uma diferença entre dar comida cozida para o animal e ele ter o desenvolvimento cultural do cozimento. Mas, ainda assim, se em todas as refeições eles tiverem acesso à comida cozida, daqui a 200 mil ou 300 mil anos eles terão o cérebro maior. Com a alimentação que têm hoje, não é possível terem um cérebro maior dado o corpo grande que têm. É uma coisa ou outra.

Somos especiais?

A gente não é especial coisa alguma. Somos apenas um primata que burlou as regras energéticas e conseguiu botar mais neurônios no cérebro de um jeito que nenhum outro animal conseguiu. Por isso estudamos os outros animais e não o contrário.

Persistem ainda mitos sobre o cérebro? Como o dos 100 bilhões de neurônios, que seus estudos demonstraram que são, na verdade, 86 bilhões?

Sim, eles continuam existindo, mesmo na neurociência. O nosso trabalho já é muito citado como referência. As coisas estão mudando. E o mais legal é que é por conta da ciência tupiniquim, o que eu acho maravilhoso. Mas vemos que é um processo, que ainda tem muita gente que insiste no número antigo.

O novo manual de diagnóstico de doenças mentais dos EUA (que serve de referência para todo o mundo, inclusive para a OMS) foi lançado na semana passada em meio à controvérsia. Especialistas acham que são tantos transtornos que praticamente não resta mais nenhum espaço para a normalidade. Qual a sua opinião?

Acho que essa discussão é muito necessária, justamente para reconhecermos o que são as variações ao redor do normal e quais são os extremos problemáticos e doentios de fato. Então, a discussão é importante, ótima a qualquer momento. Mas acho também que há muita informação errada e sensacionalista circulando, sobretudo sobre o déficit de atenção. As estatísticas variam muito de país para país, às vezes porque varia o número de médicos que reconhece a criança como portadora do distúrbio. E acho que ainda há um problema enorme, um medo enorme do estereótipo da doença mental. Até hoje ainda existe uma resistência louca em ir a um psiquiatra. E acho que, pelo contrário, ganhamos muito reconhecendo que existem transtornos e que eles podem ser tratados.

Ainda há muito estigma?

O maior problema hoje em dia é que é feio ter um distúrbio no cérebro. Perceba que nem estou falando em transtorno mental. Precisar de remédio para o cérebro é terrível. E temos tanto a ganhar reconhecendo os problemas, fazendo os diagnósticos. O cérebro é tão complexo, tem tanta coisa para dar errado, que o espantoso é que não dê problema em todo mundo sempre. Então, acho normal que boa parte da população tenha algum problema, não me espanta nem um pouco. E, uma vez que se reconhece o problema, que se faz o diagnóstico, há a opção de poder tratar. Se dispomos de um tratamento, por que não usar?

O presidente dos EUA, Barack Obama, recentemente anunciou uma inédita iniciativa de reunir pesquisadores dos mais diversos centros para estudar exclusivamente o cérebro. O que podemos esperar de tamanho esforço científico?

Não só o cérebro, mas o cérebro em atividade. Obama quer ir além do que já tinham feito — estudar a função de diferentes áreas — e entender como se conectam, como falam umas com as outras, ter ideia desse funcionamento integrado, dessa interação. Essa é uma das grandes lacunas do conhecimento: entender como as várias partes do cérebro funcionam ao mesmo tempo. Não sabemos como o cérebro funciona como um todo; é uma das fronteiras finais do conhecimento.

Não sabemos como o cérebro funciona?

Como um todo, não. Sabemos o que as partes fazem, mas não sabemos como se dá a conversa entre elas. Não sabemos a origem da consciência, da sensação do “eu estou aqui agora”. Que áreas são fundamentais para isso? É esse tipo de conhecimento que se está buscando, do cérebro funcionando ao vivo e em cores, em tempo real.

O objetivo não é estudar doenças, então?

Não, o grande objetivo é estudar consciência, memória; entender como o cérebro reúne emoção e lógica, coisas que são fruto da ação coordenada de várias partes. Claro que desse conhecimento todo podem surgir implicações para o Alzheimer e outras doenças. Mas, na verdade, falar em doenças é uma roupagem usada pela divulgação do programa para o público assimilar melhor. Existe esse preconceito de que a ciência só vale quando resolve uma doença.

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Schizophrenia Symptoms Eliminated in Animal Model (Science Daily)

May 22, 2013 — Overexpression of a gene associated with schizophrenia causes classic symptoms of the disorder that are reversed when gene expression returns to normal, scientists report. 

Overexpression of a gene associated with schizophrenia causes classic symptoms of the disorder that are reversed when gene expression returns to normal, scientists report. Pictured are (left to right) Drs. Lin Mei, Dongmin Yin and Yongjun Chen, Medical College of Georgia at Georgia Regents University. (Credit: Phil Jones, Georgia Regents University Photographer)

They genetically engineered mice so they could turn up levels of neuregulin-1 to mimic high levels found in some patients then return levels to normal, said Dr. Lin Mei, Director of the Institute of Molecular Medicine and Genetics at the Medical College of Georgia at Georgia Regents University.

They found that when elevated, mice were hyperactive, couldn’t remember what they had just learned and couldn’t ignore distracting background or white noise. When they returned neuregulin-1 levels to normal in adult mice, the schizophrenia-like symptoms went away, said Mei, corresponding author of the study in the journal Neuron.

While schizophrenia is generally considered a developmental disease that surfaces in early adulthood, Mei and his colleagues found that even when they kept neuregulin-1 levels normal until adulthood, mice still exhibited schizophrenia-like symptoms once higher levels were expressed. Without intervention, they developed symptoms at about the same age humans do.

“This shows that high levels of neuregulin-1 are a cause of schizophrenia, at least in mice, because when you turn them down, the behavior deficit disappears,” Mei said. “Our data certainly suggests that we can treat this cause by bringing down excessive levels of neuregulin-1 or blocking its pathologic effects.”

Schizophrenia is a spectrum disorder with multiple causes — most of which are unknown — that tends to run in families, and high neuregulin-1 levels have been found in only a minority of patients. To reduce neuregulin-1 levels in those individuals likely would require development of small molecules that could, for example, block the gene’s signaling pathways, Mei said. Current therapies treat symptoms and generally focus on reducing the activity of two neurotransmitters since the bottom line is excessive communication between neurons.

The good news is it’s relatively easy to measure neuregulin-1 since blood levels appear to correlate well with brain levels. To genetically alter the mice, they put a copy of the neuregulin-1 gene into mouse DNA then, to make sure they could control the levels, they put in front of the DNA a binding protein for doxycycline, a stable analogue for the antibiotic tetracycline, which is infamous for staining the teeth of fetuses and babies.

The mice are born expressing high levels of neuregulin-1 and giving the antibiotic restores normal levels. “If you don’t feed the mice tetracycline, the neuregulin-1 levels are always high,” said Mei, noting that endogenous levels of the gene are not affected. High-levels of neuregulin-1 appear to activate the kinase LIMK1, impairing release of the neurotransmitter glutamate and normal behavior. The LIMK1 connection identifies another target for intervention, Mei said.

Neuregulin-1 is essential for heart development as well as formation of myelin, the insulation around nerves. It’s among about 100 schizophrenia-associated genes identified through genome-wide association studies and has remained a consistent susceptibility gene using numerous other methods for examining the genetics of the disease. It’s also implicated in cancer.

Mei and his colleagues were the first to show neuregulin-1’s positive impact in the developed brain, reporting in Neuron in 2007 that it and its receptor ErbB4 help maintain a healthy balance of excitement and inhibition by releasing GABA, a major inhibitory neurotransmitter, at the sight of inhibitory synapses, the communication paths between neurons. Years before, they showed the genes were also at excitatory synapses, where they also could quash activation. In 2009, the MCG researchers provided additional evidence of the role of neuregulin-1 in schizophrenia by selectively deleting the gene for its receptor, ErbB4 and creating another symptomatic mouse.

Schizophrenia affects about 1 percent of the population, causing hallucinations, depression and impaired thinking and social behavior. Babies born to mothers who develop a severe infection, such as influenza or pneumonia, during pregnancy have a significantly increased risk of schizophrenia.

Journal Reference:

  1. Dong-Min Yin, Yong-Jun Chen, Yi-Sheng Lu, Jonathan C. Bean, Anupama Sathyamurthy, Chengyong Shen, Xihui Liu, Thiri W. Lin, Clifford A. Smith, Wen-Cheng Xiong, Lin Mei.Reversal of Behavioral Deficits and Synaptic Dysfunction in Mice Overexpressing Neuregulin 1.Neuron, 2013; 78 (4): 644 DOI:10.1016/j.neuron.2013.03.028

Brain Can Be Trained in Compassion, Study Shows (Science Daily)

May 22, 2013 — Until now, little was scientifically known about the human potential to cultivate compassion — the emotional state of caring for people who are suffering in a way that motivates altruistic behavior.

Investigators trained young adults to engage in compassion meditation, an ancient Buddhist technique to increase caring feelings for people who are suffering. (Credit: © byheaven / Fotolia)

A new study by researchers at the Center for Investigating Healthy Minds at the Waisman Center of the University of Wisconsin-Madison shows that adults can be trained to be more compassionate. The report, published Psychological Science, a journal of the Association for Psychological Science, investigates whether training adults in compassion can result in greater altruistic behavior and related changes in neural systems underlying compassion.

“Our fundamental question was, ‘Can compassion be trained and learned in adults? Can we become more caring if we practice that mindset?'” says Helen Weng, lead author of the study and a graduate student in clinical psychology. “Our evidence points to yes.”

In the study, the investigators trained young adults to engage in compassion meditation, an ancient Buddhist technique to increase caring feelings for people who are suffering. In the meditation, participants envisioned a time when someone has suffered and then practiced wishing that his or her suffering was relieved. They repeated phrases to help them focus on compassion such as, “May you be free from suffering. May you have joy and ease.”

Participants practiced with different categories of people, first starting with a loved one, someone whom they easily felt compassion for, like a friend or family member. Then, they practiced compassion for themselves and, then, a stranger. Finally, they practiced compassion for someone they actively had conflict with called the “difficult person,” such as a troublesome coworker or roommate.

“It’s kind of like weight training,” Weng says. “Using this systematic approach, we found that people can actually build up their compassion ‘muscle’ and respond to others’ suffering with care and a desire to help.”

Compassion training was compared to a control group that learned cognitive reappraisal, a technique where people learn to reframe their thoughts to feel less negative. Both groups listened to guided audio instructions over the Internet for 30 minutes per day for two weeks. “We wanted to investigate whether people could begin to change their emotional habits in a relatively short period of time,” says Weng.

The real test of whether compassion could be trained was to see if people would be willing to be more altruistic — even helping people they had never met. The research tested this by asking the participants to play a game in which they were given the opportunity to spend their own money to respond to someone in need (called the “Redistribution Game”). They played the game over the Internet with two anonymous players, the “Dictator” and the “Victim.” They watched as the Dictator shared an unfair amount of money (only $1 out of $10) with the Victim. They then decided how much of their own money to spend (out of $5) in order to equalize the unfair split and redistribute funds from the Dictator to the Victim.

“We found that people trained in compassion were more likely to spend their own money altruistically to help someone who was treated unfairly than those who were trained in cognitive reappraisal,” Weng says.

“We wanted to see what changed inside the brains of people who gave more to someone in need. How are they responding to suffering differently now?” asks Weng. The study measured changes in brain responses using functional magnetic resonance imaging (fMRI) before and after training. In the MRI scanner, participants viewed images depicting human suffering, such as a crying child or a burn victim, and generated feelings of compassion towards the people using their practiced skills. The control group was exposed to the same images, and asked to recast them in a more positive light as in reappraisal.

The researchers measured how much brain activity had changed from the beginning to the end of the training, and found that the people who were the most altruistic after compassion training were the ones who showed the most brain changes when viewing human suffering. They found that activity was increased in the inferior parietal cortex, a region involved in empathy and understanding others. Compassion training also increased activity in the dorsolateral prefrontal cortex and the extent to which it communicated with the nucleus accumbens, brain regions involved in emotion regulation and positive emotions.

“People seem to become more sensitive to other people’s suffering, but this is challenging emotionally. They learn to regulate their emotions so that they approach people’s suffering with caring and wanting to help rather than turning away,” explains Weng.

Compassion, like physical and academic skills, appears to be something that is not fixed, but rather can be enhanced with training and practice. “The fact that alterations in brain function were observed after just a total of seven hours of training is remarkable,” explains UW-Madison psychology and psychiatry professor Richard J. Davidson, founder and chair of the Center for Investigating Healthy Minds and senior author of the article.

“There are many possible applications of this type of training,” Davidson says. “Compassion and kindness training in schools can help children learn to be attuned to their own emotions as well as those of others, which may decrease bullying. Compassion training also may benefit people who have social challenges such as social anxiety or antisocial behavior.”

Weng is also excited about how compassion training can help the general population. “We studied the effects of this training with healthy participants, which demonstrated that this can help the average person. I would love for more people to access the training and try it for a week or two — what changes do they see in their own lives?”

Both compassion and reappraisal trainings are available on the Center for Investigating Healthy Minds’ website. “I think we are only scratching the surface of how compassion can transform people’s lives,” says Weng.

Other authors on the paper were Andrew S. Fox, Alexander J. Shackman, Diane E. Stodola, Jessica Z. K. Caldwell, Matthew C. Olson, and Gregory M. Rogers.

The work was supported by funds from the National Institutes of Health; a Hertz Award to the UW-Madison Department of Psychology; the Fetzer Institute; The John Templeton Foundation; the Impact Foundation; the J. W. Kluge Foundation; the Mental Insight Foundation; the Mind and Life Institute; and gifts from Bryant Wanguard, Ralph Robinson, and Keith and Arlene Bronstein.

Journal Reference:

  1. H. Y. Weng, A. S. Fox, A. J. Shackman, D. E. Stodola, J. Z. K. Caldwell, M. C. Olson, G. M. Rogers, R. J. Davidson.Compassion Training Alters Altruism and Neural Responses to SufferingPsychological Science, 2013; DOI: 10.1177/0956797612469537

Tamed fox shows domestication’s effects on the brain (Science News)

Gene activity changes accompany doglike behavior

By Tina Hesman Saey

Web edition: May 15, 2013

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Taming silver foxes (shown) alters their behavior. A new study links those behavior changes to changes in brain chemicals. Tom Reichner/Shutterstock

COLD SPRING HARBOR, N.Y. – Taming foxes changes not only the animals’ behavior but also their brain chemistry, a new study shows.

The finding could shed light on how the foxes’ genetic cousins, wolves, morphed into man’s best friend. Lenore Pipes of Cornell University presented the results May 10 at the Biology of Genomes conference.

The foxes she worked with come from a long line started in 1959 when a Russian scientist named Dmitry Belyaev attempted to recreate dog domestication, but using foxes instead of wolves. He bred silver foxes (Vulpes vulpes), which are actually a type of red fox with white-tipped black fur. Belyaev and his colleagues selected the least aggressive animals they could find at local fox farms and bred them. Each generation, the scientists picked the tamest animals to mate, creating ever friendlier foxes. Now, more than 50 years later, the foxes act like dogs, wagging their tails, jumping with excitement and leaping into the arms of caregivers for caresses.

At the same time, the scientists also bred the most aggressive foxes on the farms. The descendents of those foxes crouch, flatten their ears, growl, bare their teeth and lunge at people who approach their cages.

The foxes’ tame and aggressive behaviors are rooted in genetics, but scientists have not found DNA changes that account for the differences. Rather than search for changes in genes themselves, Pipes and her colleagues took an indirect approach, looking for differences in the activity of genes in the foxes’ brains.

The team collected two brain parts, the prefrontal cortex and amygdala, from a dozen aggressive foxes and a dozen tame ones. The prefrontal cortex, an area at the front of the brain, is involved in decision making and in controlling social behavior, among other tasks. The amygdala, a pair of almond-size regions on either side of the brain, helps process emotional information.

Pipes found that the activity of hundreds of genes in the two brain regions differed between the groups of affable and hostile foxes. For example, aggressive animals had increased activity of some genes for sensing dopamine. Pipes speculated that tame animals’ lower levels of dopamine sensors might make them less anxious.

The team had expected to find changes in many genes involved in serotonin signaling, a process targeted by some popular antidepressants such as Prozac. Tame foxes are known to have more serotonin in their brains. But only one gene for sensing serotonin had higher activity in the friendly animals.

In a different sort of analysis, Pipes discovered that all aggressive foxes carry one form of the GRM3 glutamate receptor gene, while a majority of the friendly foxes have a different variant of the gene. In people, genetic variants of GRM3 have been linked to schizophrenia, bipolar disorder and other mood disorders. Other genes involved in transmitting glutamate signals, which help regulate mood, had increased activity in tame foxes, Pipes said.

It is not clear whether similar brain chemical changes accompanied the transformation of wolves into dogs, said Adam Freedman, an evolutionary biologist at Harvard University. Even if dogs and wolves now have differing brain chemical levels, researchers can’t turn back time to watch the process unfold; they can only guess at how domestication happened. “We have to reconstruct an unobservable series of steps,” he said. Pipes’ study is an interesting example of what might have happened to dogs’ brains during domestication, he said.

Clouds in the Head: New Model of Brain’s Thought Processes (Science Daily)

May 21, 2013 — A new model of the brain’s thought processes explains the apparently chaotic activity patterns of individual neurons. They do not correspond to a simple stimulus/response linkage, but arise from the networking of different neural circuits. Scientists funded by the Swiss National Science Foundation (SNSF) propose that the field of brain research should expand its focus.

A new model of the brain’s thought processes explains the apparently chaotic activity patterns of individual neurons. They do not correspond to a simple stimulus/response linkage, but arise from the networking of different neural circuits. (Credit: iStockphoto/Sebastian Kaulitzki)

Many brain researchers cannot see the forest for the trees. When they use electrodes to record the activity patterns of individual neurons, the patterns often appear chaotic and difficult to interpret. “But when you zoom out from looking at individual cells, and observe a large number of neurons instead, their global activity is very informative,” says Mattia Rigotti, a scientist at Columbia University and New York University who is supported by the SNSF and the Janggen-Pöhn-Stiftung. Publishing inNature together with colleagues from the United States, he has shown that these difficult-to-interpret patterns in particular are especially important for complex brain functions.

What goes on in the heads of apes

The researchers have focussed their attention on the activity patterns of 237 neurons that had been recorded some years previously using electrodes implanted in the frontal lobes of two rhesus monkeys. At that time, the apes had been taught to recognise images of different objects on a screen. Around one third of the observed neurons demonstrated activity that Rigotti describes as “mixed selectivity.” A mixed selective neuron does not always respond to the same stimulus (the flowers or the sailing boat on the screen) in the same way. Rather, its response differs as it also takes account of the activity of other neurons. The cell adapts its response according to what else is going on in the ape’s brain.

Chaotic patterns revealed in context

Just as individual computers are networked to create concentrated processing and storage capacity in the field of Cloud Computing, links in the complex cognitive processes that take place in the prefrontal cortex play a key role. The greater the density of the network in the brain, in other words the greater the proportion of mixed selectivity in the activity patterns of the neurons, the better the apes were able to recall the images on the screen, as demonstrated by Rigotti in his analysis. Given that the brain and cognitive capabilities of rhesus monkeys are similar to those of humans, mixed selective neurons should also be important in our own brains. For him this is reason enough why brain research from now on should no longer be satisfied with just the simple activity patterns, but should also consider the apparently chaotic patterns that can only be revealed in context.

Journal Reference:

  1. Mattia Rigotti, Omri Barak, Melissa R. Warden, Xiao-Jing Wang, Nathaniel D. Daw, Earl K. Miller, Stefano Fusi. The importance of mixed selectivity in complex cognitive tasksNature, 2013; DOI: 10.1038/nature12160

Major Depression: Great Success With Pacemaker Electrodes, Small Study Suggests (Science Daily)

Apr. 9, 2013 — Researchers from the Bonn University Hospital implanted pacemaker electrodes into the medial forebrain bundle in the brains of patients suffering from major depression with amazing results: In six out of seven patients, symptoms improved both considerably and rapidly. The method of Deep Brain Stimulation had already been tested on various structures within the brain, but with clearly lesser effect.

The medial forebrain bundle is highlighted in green. (Credit: Volker Arnd Coenen/Uni Freiburg)

The results of this new study have now been published in the international journal Biological Psychiatry.

After months of deep sadness, a first smile appears on a patient’s face. For many years, she had suffered from major depression and tried to end her life several times. She had spent the past years mostly in a passive state on her couch; even watching TV was too much effort for her. Now this young woman has found her joie de vivre again, enjoys laughing and travelling. She and an additional six patients with treatment resistant depression participated in a study involving a novel method for addressing major depression at the Bonn University Hospital.

Considerable amelioration of depression within days

Prof. Dr. Volker Arnd Coenen, neurosurgeon at the Department of Neurosurgery (Klinik und Poliklinik für Neurochirurgie), implanted electrodes into the medial forebrain bundles in the brains of subjects suffering from major depression with the electrodes being connected to a brain pacemaker. The nerve cells were then stimulated by means of a weak electrical current, a method called Deep Brain Stimulation. In a matter of days, in six out of seven patients, symptoms such as anxiety, despondence, listlessness and joylessness had improved considerably. “Such sensational success both in terms of the strength of the effects, as well as the speed of the response has so far not been achieved with any other method,” says Prof. Dr. Thomas E. Schläpfer from the Bonn University Hospital Department of Psychiatry und Psychotherapy (Bonner Uniklinik für Psychiatrie und Psychotherapie).

Central part of the reward circuit

The medial forebrain bundle is a bundle of nerve fibers running from the deep-seated limbic system to the prefrontal cortex. In a certain place, the bundle is particularly narrow because the individual nerve fibers lie close together. “This is exactly the location in which we can have maximum effect using a minimum of current,” explains Prof. Coenen, who is now the new head of the Freiburg University Hospital’s Department of Stereotactic and Functional Neurosurgery (Abteilung Stereotaktische und Funktionelle Neurochirurgie am Universitätsklinikum Freiburg). The medial forebrain bundle is a central part of a euphoria circuit belonging to the brain’s reward system. What kind of effect stimulation exactly has on nerve cells is not yet known. But it obviously changes metabolic activity in the different brain centers.

Success clearly increased over that of earlier studies

The researchers have already shown in several studies that deep brain stimulation shows an amazing and-given the severity of the symptoms- unexpected degree of amelioration of symptoms in major depression. In those studies, however, the physicians had not implanted the electrodes into the medial forebrain bundle but instead into the nucleus accumbens, another part of the brain’s reward system. This had resulted in clear and sustainable improvements in about 50 percent of subjects. “But in this new study, our results were even much better,” says Prof. Schläpfer. A clear improvement in complaints was found in 85 percent of patients, instead of the earlier 50 percent. In addition, stimulation was performed with lower current levels, and the effects showed within a few days, instead of after weeks.

Method’s long-term success

“Obviously, we have now come closer to a critical structure within the brain that is responsible for major depression,” says the psychiatrist from the Bonn University Hospital. Another cause for optimism among the group of physicians is that, since the study’s completion, an eighth patient has also been treated successfully. The patients have been observed for a period of up to 18 month after the intervention. Prof. Schläpfer reports, “The anti-depressive effect of deep brain stimulation within the medial forebrain bundle has not decreased during this period.” This clearly indicates that the effects are not temporary. This method gives those who suffer from major depression reason to hope. However, it will take quite a bit of time for the new procedure to become part of standard therapy.

Journal Reference:

  1. Thomas E. Schlaepfer, Bettina H. Bewernick, Sarah Kayser, Burkhard Mädler, Volker A. Coenen. Rapid Effects of Deep Brain Stimulation for Treatment-Resistant Major DepressionBiological Psychiatry, 2013; DOI:10.1016/j.biopsych.2013.01.034

Mind Over Matter? Core Body Temperature Controlled by the Brain (Science Daily)

Apr. 8, 2013 — A team of researchers led by Associate Professor Maria Kozhevnikov from the Department of Psychology at the National University of Singapore (NUS) Faculty of Arts and Social Sciences showed, for the first time, that it is possible for core body temperature to be controlled by the brain. The scientists found that core body temperature increases can be achieved using certain meditation techniques (g-tummo) which could help in boosting immunity to fight infectious diseases or immunodeficiency.

Meditation. (Credit: © Yuri Arcurs / Fotolia)

Published in science journal PLOS ONE in March 2013, the study documented reliable core body temperature increases for the first time in Tibetan nuns practising g-tummo meditation. Previous studies on g-tummo meditators showed only increases in peripheral body temperature in the fingers and toes. The g-tummo meditative practice controls “inner energy” and is considered by Tibetan practitioners as one of the most sacred spiritual practices in the region. Monasteries maintaining g-tummo traditions are very rare and are mostly located in the remote areas of eastern Tibet.

The researchers collected data during the unique ceremony in Tibet, where nuns were able to raise their core body temperature and dry up wet sheets wrapped around their bodies in the cold Himalayan weather (-25 degree Celsius) while meditating. Using electroencephalography (EEG) recordings and temperature measures, the team observed increases in core body temperature up to 38.3 degree Celsius. A second study was conducted with Western participants who used a breathing technique of the g-tummo meditative practice and they were also able to increase their core body temperature, within limits.

Applications of the research findings

The findings from the study showed that specific aspects of the meditation techniques can be used by non-meditators to regulate their body temperature through breathing and mental imagery. The techniques could potentially allow practitioners to adapt to and function in cold environments, improve resistance to infections, boost cognitive performance by speeding up response time and reduce performance problems associated with decreased body temperature.

The two aspects of g-tummo meditation that lead to temperature increases are “vase breath” and concentrative visualisation. “Vase breath” is a specific breathing technique which causes thermogenesis, which is a process of heat production. The other technique, concentrative visualisation, involves focusing on a mental imagery of flames along the spinal cord in order to prevent heat losses. Both techniques work in conjunction leading to elevated temperatures up to the moderate fever zone.

Assoc Prof Kozhevnikov explained, “Practicing vase breathing alone is a safe technique to regulate core body temperature in a normal range. The participants whom I taught this technique to were able to elevate their body temperature, within limits, and reported feeling more energised and focused. With further research, non-Tibetan meditators could use vase breathing to improve their health and regulate cognitive performance.”

Further research into controlling body temperature

Assoc Prof Kozhevnikov will continue to explore the effects of guided imagery on neurocognitive and physiological aspects. She is currently training a group of people to regulate their body temperature using vase breathing, which has potential applications in the field of medicine. Furthermore, the use of guided mental imagery in conjunction with vase breathing may lead to higher body temperature increases and better health.

Journal Reference:

  1. Maria Kozhevnikov, James Elliott, Jennifer Shephard, Klaus Gramann. Neurocognitive and Somatic Components of Temperature Increases during g-Tummo Meditation: Legend and RealityPLoS ONE, 2013; 8 (3): e58244 DOI:10.1371/journal.pone.0058244

How Our Bodies Interact With Our Minds in Response to Fear and Other Emotions (Science Daily)

Apr. 7, 2013 — New research has shown that the way our minds react to and process emotions such as fear can vary according to what is happening in other parts of our bodies.

New research has shown that the way our minds react to and process emotions such as fear can vary according to what is happening in other parts of our bodies. (Credit: © sellingpix / Fotolia)

In two different presentations on April 8 at the British Neuroscience Association Festival of Neuroscience (BNA2013) in London, researchers have shown for the first time that the heart’s cycle affects the way we process fear, and that a part of the brain that responds to stimuli, such as touch, felt by other parts of the body also plays a role.

Dr Sarah Garfinkel, a postdoctoral fellow at the Brighton and Sussex Medical School (Brighton, UK), told a news briefing: “Cognitive neuroscience strives to understand how biological processes interact to create and influence the conscious mind. While neural activity in the brain is typically the focus of research, there is a growing appreciation that other bodily organs interact with brain function to shape and influence our perceptions, cognitions and emotions.

“We demonstrate for the first time that the way in which we process fear is different dependent on when we see fearful images in relation to our heart.”

Dr Garfinkel and her colleagues hooked up 20 healthy volunteers to heart monitors, which were linked to computers. Images of fearful faces were shown on the computers and the electrocardiography (ECG) monitors were able to communicate with the computers in order to time the presentation of the faces with specific points in the heart’s cycle.

“Our results show that if we see a fearful face during systole (when the heart is pumping) then we judge this fearful face as more intense than if we see the very same fearful face during diastole (when the heart is relaxed). To look at neural activity underlying this effect, we performed this experiment in an MRI [magnetic resonance imaging] scanner and demonstrated that a part of the brain called the amygdala influences how our heart changes our perception of fear.

“From previous research, we know that if we present images very fast then we have trouble detecting them, but if an image is particularly emotional then it can ‘pop’ out and be seen. In a second experiment, we exploited our cardiac effect on emotion to show that our conscious experience is affected by our heart. We demonstrated that fearful faces are better detected at systole (when they are perceived as more fearful), relative to diastole. Thus our hearts can also affect what we see and what we don’t see — and can guide whether we see fear.

“Lastly, we have demonstrated that the degree to which our hearts can change the way we see and process fear is influenced by how anxious we are. The anxiety level of our individual subjects altered the extent their hearts could change the way they perceived emotional faces and also altered neural circuitry underlying heart modulation of emotion.”

Dr Garfinkel says that her findings might have the potential to help people who suffer from anxiety or other conditions such as post traumatic stress disorder (PTSD).

“We have identified an important mechanism by which the heart and brain ‘speak’ to each other to change our emotions and reduce fear. We hope to explore the therapeutic implications in people with high anxiety. Anxiety disorders can be debilitating and are very prevalent in the UK and elsewhere. We hope that by increasing our understanding about how fear is processed and ways that it could be reduced, we may be able to develop more successful treatments for these people, and also for those, such as war veterans, who may be suffering from PTSD.

“In addition, there is a growing appreciation about how different forms of meditation can have therapeutic consequences. Work that integrates body, brain and mind to understand changes in emotion can help us understand how meditation and mindfulness practices can have calming effects.”

In a second presentation, Dr Alejandra Sel, a postdoctoral researcher in the Department of Psychology at City University (London, UK), investigated a part of the brain called the somatosensory cortex — the area that perceives bodily sensations, such as touch, pain, body temperature and the perception of the body’s place in space, and which is activated when we observe emotional expressions in the faces of other people.

“In order to understand other’s people emotions we need to experience the same observed emotions in our body. Specifically, observing an emotional face, as opposed to a neutral face, is associated with an increased activity in the somatosensory cortex as if we were expressing and experiencing our own emotions. It is also known that people with damage to the somatosensory cortex find it difficult to recognise emotion in other people’s faces,” Dr Sel told the news briefing.

However, until now, it has not been clear whether activity in the somatosensory cortex was simply a by-product of the way we process visual information, or whether it reacts independently to emotions expressed in other people’s faces, actively contributing to how we perceive emotions in others.

In order to discover whether the somatosensory cortex contributes to the processing of emotion independently of any visual processes, Dr Sel and her colleagues tested two situations on volunteers. Using electroencephalography (EEG) to measure the brain response to images, they showed participants either a face showing fear (emotional) or a neutral face. Secondly, they combined the showing of the face with a small tap to an index finger or the left cheek immediately afterwards.

Dr Sel said: “By tapping someone’s cheek or finger you can modify the ‘resting state’ of the somatosensory cortex inducing changes in brain electrical activity in this area. These changes are measureable and observable with EEG and this enables us to pinpoint the brain activity that is specifically related to the somatosensory cortex and its reaction to external stimuli.

“If the ‘resting state’ of the somatosensory cortex when a fearful face is shown has greater electrical activity than when a neutral face is shown, the changes in the activity of the somatosensory cortex induced by the taps and measured by EEG also will be greater when observing fearful as opposed to neutral faces.

“We subtracted results of the first situation (face only) from the second situation (face and tap), and compared changes in the activity related with the tap in the somatosensory cortex when seeing emotional faces versus neutral faces. This way, we could observe responses of the somatosensory cortex to emotional faces independently of visual processes,” she explained.

The researchers found that there was enhanced activity in the somatosensory cortex in response to fearful faces in comparison to neutral faces, independent of any visual processes. Importantly, this activity was focused in the primary and secondary somatosensory areas; the primary area receives sensory information directly from the body, while the secondary area combines sensory information from the body with information related to body movement and other information, such as memories of previous, sensitive experiences.

“Our experimental approach allows us to isolate and show for the first time (as far as we are aware) changes in somatosensory activity when seeing emotional faces after taking away all visual information in the brain. We have shown the crucial role of the somatosensory cortex in the way our minds and bodies perceive human emotions. These findings can serve as starting point for developing interventions tailored for people with problems in recognising other’s emotions, such as autistic children,” said Dr Sel.

The researchers now plan to investigate whether they get similar results when people are shown faces with other expressions such as happy or angry, and whether the timing of the physical stimulus, the tap to the finger or cheek, makes any difference. In this experiment, the tap occurred 105 milliseconds after a face was shown, and Dr Sel wonders about the effect of a longer time interval.

Story Source:

The above story is reprinted from materials provided byBritish Neuroscience Association, via AlphaGalileo.

Brain’s Stress Circuits Undergo Profound Learning Early in Life, Scientists Find (Science Daily)

Apr. 7, 2013 — Researchers at the University of Calgary’s Hotchkiss Brain Institute have discovered that stress circuits in the brain undergo profound learning early in life. Using a number of cutting edge approaches, including optogenetics, Jaideep Bains, PhD, and colleagues have shown stress circuits are capable of self-tuning following a single stress. These findings demonstrate that the brain uses stress experience during early life to prepare and optimize for subsequent challenges.

Newborn baby. Stress circuits in the brain undergo profound learning early in life. (Credit: © Iosif Szasz-Fabian / Fotolia)

The team was able to show the existence of unique time windows following brief stress challenges during which learning is either increased or decreased. By manipulating specific cellular pathways, they uncovered the key players responsible for learning in stress circuits in an animal model. These discoveries culminated in the publication of two back-to-back studies in the April 7 online edition ofNature Neuroscience.

“These new findings demonstrate that systems thought to be ‘hardwired’ in the brain, are in fact flexible, particularly early in life,” says Bains, a professor in the Department of Physiology and Pharmacology. “Using this information, researchers can now ask questions about the precise cellular and molecular links between early life stress and stress vulnerability or resilience later in life.”

Stress vulnerability, or increased sensitivity to stress, has been implicated in numerous health conditions including cardiovascular disease, obesity, diabetes and depression. Although these studies used animal models, similar mechanisms mediate disease progression in humans.

“Our observations provide an important foundation for designing more effective preventative and therapeutic strategies that mitigate the effects of stress and meet society’s health challenges,” he says.

Journal References:

  1. Wataru Inoue, Dinara V Baimoukhametova, Tamás Füzesi, Jaclyn I Wamsteeker Cusulin, Kathrin Koblinger, Patrick J Whelan, Quentin J Pittman, Jaideep S Bains.Noradrenaline is a stress-associated metaplastic signal at GABA synapsesNature Neuroscience, 2013; DOI:10.1038/nn.3373
  2. Jaclyn I Wamsteeker Cusulin, Tamás Füzesi, Wataru Inoue, Jaideep S Bains. Glucocorticoid feedback uncovers retrograde opioid signaling at hypothalamic synapsesNature Neuroscience, 2013; DOI:10.1038/nn.3374

Brain scans can now tell who you’re thinking about (Singularity Hub)

Written By: 

Posted: 03/23/13 7:48 AM

[Source: Listal]

[Source: Listal]

Beware stalkers, these neuroscientists can tell who you’re thinking of. Or, at least, the kind of personality he or she might have.

As a social species humans are highly attuned to the behavior of others around them. It’s a survival mechanism, helping us to safely navigate the social world. That awareness involves both evaluating people and predicting how they will behave in different situations in the future (“Uh oh, don’t get him started!”). But just how does the brain represent another person’s personality?

To answer this question a group of scientists at Cornell’s College of Human Ecology (whatever that means) used functional magnetic resonance imaging (fMRI) to measure neuronal activity while people thought about different types of personalities. The 19 participants – all young adults – learned about four protagonists, all of whom had considerably different personalities, based on agreeableness (e.g., “Likes to cooperate with others”) and extraversion (“Is sometimes shy”). They were then presented different scenarios (such as sitting on a bus with no empty seats and watching an elderly person get on) and asked to imagine how each of the four protagonists would react.

Varying degrees of a person's deemed "agreeableness" and "extraversion" combine to produce different brain activation patterns in the brain. [Source: Cerebral Cortex]

Varying degrees of a person’s deemed “agreeableness” and “extraversion” combine to produce different brain activation patterns in the brain. [Source: Cerebral Cortex]

The study’s lead author, Nathan Spreng, said they were “shocked” when they saw the results. The brain scans revealed that each of the four distinct personalities elicited four distinct activity patterns in the medial prefrontal cortex, an area at the front of the brain known to be involved in decision making. In essence, the researchers had succeeded in extracting mental pictures – the personalities of others – that people were thinking of.The study was published in the March 5 issue of Cerebral Cortex.

Sizing up the personality of another or thinking what they’re thinking is unique to social animals and in fact to do so was until recently thought to be uniquely human. But there’s now reason to believe the network – called the ‘default network’ – is a fundamental feature of social mammals in general. As Spreng explained in an email, “Macaque [monkeys] clearly have a similar network, observable even in the rat. All of these mammalian species are highly social.”

The fact that the mental snapshot of others was seen in the neurons of the medial prefrontal cortex means the current study may have implications for autism, Spreng said in a Cornell University news release. “Prior research has implicated the anterior mPFC in social cognition disorders such as autism, and our results suggest people with such disorders may have an inability to build accurate personality models. If further research bears this out, we may ultimately be able to identify specific brain activation biomarkers not only for diagnosing such diseases, but for monitoring the effects of interventions.”

Previous work has shown that brain scans can tell us a lot about what a person’s thinking. With an array of electrodes placed directly on the brain, researchers were able to decode specific words that people were thinking. In another experiment fRMI scans of the visual cortex were used to reconstruct movie trailers that participants were watching.

Much of neuroscience explores how the brain processes the sensory information that guides us through our physical environment. But, for many species, navigating the social environment can be just as important to survival. “For me, an important feature of the work is that our emotions and thoughts about other people are felt to be private experiences,” Spreng said. “In our life, we may choose to share our thoughts and feelings with peers, friends and loved ones. However, [thoughts and feelings] are also physical and biological processes that can be observed. Considering how important our social world is, we know very little about the brain processes that support social knowledge. The objective of this work is to understand the physical mechanisms that allow us to have an inner world, and a part of that is how we represent other people in our mind.”

Brain Scans Predict Which Criminals Are Most Likely to Reoffend (Wired)

BY GREG MILLER

03.26.13 – 3:40 PM

Photo: Erika Kyte/Getty Images

Brain scans of convicted felons can predict which ones are most likely to get arrested after they get out of prison, scientists have found in a study of 96 male offenders.

“It’s the first time brain scans have been used to predict recidivism,” said neuroscientist Kent Kiehl of the Mind Research Network in Albuquerque, New Mexico, who led the new study. Even so, Kiehl and others caution that the method is nowhere near ready to be used in real-life decisions about sentencing or parole.

Generally speaking, brain scans or other neuromarkers could be useful in the criminal justice system if the benefits in terms of better accuracy outweigh the likely higher costs of the technology compared to conventional pencil-and-paper risk assessments, says Stephen Morse, a legal scholar specializing in criminal law and neuroscience at the University of Pennsylvania. The key questions to ask, Morse says, are: “How much predictive accuracy does the marker add beyond usually less expensive behavioral measures? How subject is it to counter-measures if a subject wishes to ‘defeat’ a scan?”

Those are still open questions with regard to the new method, which Kiehl and colleagues, including postdoctoral fellow Eyal Aharoni, describe in a paper to be published this week in the Proceedings of the National Academy of Sciences.

The test targets impulsivity. In a mobile fMRI scanner the researchers trucked in to two state prisons, they scanned inmates’ brains as they did a simple impulse control task. Inmates were instructed to press a button as quickly as possible whenever they saw the letter X pop up on a screen inside the scanner, but not to press it if they saw the letter K. The task is rigged so that X pops up 84 percent of the time, which predisposes people to hit the button and makes it harder to suppress the impulse to press the button on the rare trials when a K pops up.

Based on previous studies, the researchers focused on the anterior cingulate cortex, one of several brain regions thought to be important for impulse control. Inmates with relatively low activity in the anterior cingulate made more errors on the task, suggesting a correlation with poor impulse control.

They were also more likely to get arrested after they were released. Inmates with relatively low anterior cingulate activity were roughly twice as likely as inmates with high anterior cingulate activity to be rearrested for a felony offense within 4 years of their release, even after controlling for other behavioral and psychological risk factors.

“This is an exciting new finding,” said Essi Viding, a professor of developmental psychopathology at University College London. “Interestingly this brain activity measure appears to be a more robust predictor, in particular of non-violent offending, than psychopathy or drug use scores, which we know to be associated with a risk of reoffending.” However, Viding notes that Kiehl’s team hasn’t yet tried to compare their fMRI test head to head against pencil-and-paper tests specifically designed to assess the risk of recidivism. ”It would be interesting to see how the anterior cingulate cortex activity measure compares against these measures,” she said.

“It’s a great study because it brings neuroimaging into the realm of prediction,” said clinical psychologistDustin Pardini of the University of Pittsburgh. The study’s design is an improvement over previous neuroimaging studies that compared groups of offenders with groups of non-offenders, he says. All the same, he’s skeptical that brain scans could be used to predict the behavior of a given individual. ”In general we’re horrible at predicting human behavior, and I don’t see this as being any different, at least not in the near future.”

Even if the findings hold up in a larger study, there would be limitations, Pardini adds. “In a practical sense, there are just too many ways an offender could get around having an accurate representation of his brain activity taken,” he said. For example, if an offender moves his head while inside the scanner, that would render the scan unreadable. Even more subtle strategies, such as thinking about something unrelated to the task, or making mistakes on purpose, could also thwart the test.

Kiehl isn’t convinced either that this type of fMRI test will ever prove useful for assessing the risk to society posed by individual criminals. But his group is collecting more data — lots more — as part of a much larger study in the New Mexico state prisons. “We’ve scanned 3,000 inmates,” he said. “This is just the first 100.”

Kiehl hopes this work will point to new strategies for reducing criminal behavior. If low activity in the anterior cingulate does in fact turn out to be a reliable predictor of recidivism, perhaps therapies that boost activity in this region would improve impulse control and prevent future crimes, Kiehl says. He admits it’s speculative, but his group is already thinking up experiments to test the idea. ”Cognitive exercises is where we’ll start,” he said. “But I wouldn’t rule out pharmaceuticals.”

DNA Damage Occurs as Part of Normal Brain Activity, Scientists Discover (Science Daily)

Mar. 24, 2013 — Scientists at the Gladstone Institutes have discovered that a certain type of DNA damage long thought to be particularly detrimental to brain cells can actually be part of a regular, non-harmful process. The team further found that disruptions to this process occur in mouse models of Alzheimer’s disease — and identified two therapeutic strategies that reduce these disruptions.

Neurons. Scientists have discovered that a certain type of DNA damage long thought to be particularly detrimental to brain cells can actually be part of a regular, non-harmful process. (Credit: © Roberto Robuffo / Fotolia)

Scientists have long known that DNA damage occurs in every cell, accumulating as we age. But a particular type of DNA damage, known as a double-strand break, or DSB, has long been considered a major force behind age-related illnesses such as Alzheimer’s. Today, researchers in the laboratory of Gladstone Senior Investigator Lennart Mucke, MD, report in Nature Neuroscience that DSBs in neuronal cells in the brain can also be part of normal brain functions such as learning — as long as the DSBs are tightly controlled and repaired in good time. Further, the accumulation of the amyloid-beta protein in the brain — widely thought to be a major cause of Alzheimer’s disease — increases the number of neurons with DSBs and delays their repair.

“It is both novel and intriguing team’s finding that the accumulation and repair of DSBs may be part of normal learning,” said Fred H. Gage, PhD, of the Salk Institute who was not involved in this study. “Their discovery that the Alzheimer’s-like mice exhibited higher baseline DSBs, which weren’t repaired, increases these findings’ relevance and provides new understanding of this deadly disease’s underlying mechanisms.”

In laboratory experiments, two groups of mice explored a new environment filled with unfamiliar sights, smells and textures. One group was genetically modified to simulate key aspects of Alzheimer’s, and the other was a healthy, control group. As the mice explored, their neurons became stimulated as they processed new information. After two hours, the mice were returned to their familiar, home environment.

The investigators then examined the neurons of the mice for markers of DSBs. The control group showed an increase in DSBs right after they explored the new environment — but after being returned to their home environment, DSB levels dropped.

“We were initially surprised to find neuronal DSBs in the brains of healthy mice,” said Elsa Suberbielle, DVM, PhD, Gladstone postdoctoral fellow and the paper’s lead author. “But the close link between neuronal stimulation and DSBs, and the finding that these DSBs were repaired after the mice returned to their home environment, suggest that DSBs are an integral part of normal brain activity. We think that this damage-and-repair pattern might help the animals learn by facilitating rapid changes in the conversion of neuronal DNA into proteins that are involved in forming memories.”

The group of mice modified to simulate Alzheimer’s had higher DSB levels at the start — levels that rose even higher during neuronal stimulation. In addition, the team noticed a substantial delay in the DNA-repair process.

To counteract the accumulation of DSBs, the team first used a therapeutic approach built on two recent studies — one of which was led by Dr. Mucke and his team — that showed the widely used anti-epileptic drug levetiracetam could improve neuronal communication and memory in both mouse models of Alzheimer’s and in humans in the disease’s earliest stages. The mice they treated with the FDA-approved drug had fewer DSBs. In their second strategy, they genetically modified mice to lack the brain protein called tau — another protein implicated in Alzheimer’s. This manipulation, which they had previously found to prevent abnormal brain activity, also prevented the excessive accumulation of DSBs.

The team’s findings suggest that restoring proper neuronal communication is important for staving off the effects of Alzheimer’s — perhaps by maintaining the delicate balance between DNA damage and repair.

“Currently, we have no effective treatments to slow, prevent or halt Alzheimer’s, from which more than 5 million people suffer in the United States alone,” said Dr. Mucke, who directs neurological research at Gladstone and is a professor of neuroscience and neurology at the University of California, San Francisco, with which Gladstone is affiliated. “The need to decipher the causes of Alzheimer’s and to find better therapeutic solutions has never been more important — or urgent. Our results suggest that readily available drugs could help protect neurons against some of the damages inflicted by this illness. In the future, we will further explore these therapeutic strategies. We also hope to gain a deeper understanding of the role that DSBs play in learning and memory — and in the disruption of these important brain functions by Alzheimer’s disease.”

Other scientists who participated in this research at Gladstone include Pascal Sanchez, PhD, Alexxai Kravitz, PhD, Xin Wang, Kaitlyn Ho, Kirsten Eilertson, PhD, Nino Devidze, PhD, and Anatol Kreitzer, PhD. This research was supported by grants from the National Institutes of Health and the S.D. Bechtel, Jr. Foundation.

Journal Reference:

  1. Elsa Suberbielle, Pascal E Sanchez, Alexxai V Kravitz, Xin Wang, Kaitlyn Ho, Kirsten Eilertson, Nino Devidze, Anatol C Kreitzer, Lennart Mucke. Physiologic brain activity causes DNA double-strand breaks in neurons, with exacerbation by amyloid-βNature Neuroscience, 2013; DOI: 10.1038/nn.3356

Red Brain, Blue Brain: Republicans and Democrats Process Risk Differently, Research Finds (Science Daily)

Feb. 13, 2013 — A team of political scientists and neuroscientists has shown that liberals and conservatives use different parts of the brain when they make risky decisions, and these regions can be used to predict which political party a person prefers. The new study suggests that while genetics or parental influence may play a significant role, being a Republican or Democrat changes how the brain functions.

Republicans and Democrats differ in the neural mechanisms activated while performing a risk-taking task. Republicans more strongly activate their right amygdala, associated with orienting attention to external cues. Democrats have higher activity in their left posterior insula, associated with perceptions of internal physiological states. This activation also borders the temporal-parietal junction, and therefore may reflect a difference in internal physiological drive as well as the perception of the internal state and drive of others. (Credit: From: Darren Schreiber, Greg Fonzo, Alan N. Simmons, Christopher T. Dawes, Taru Flagan, James H. Fowler, Martin P. Paulus. Red Brain, Blue Brain: Evaluative Processes Differ in Democrats and Republicans. PLoS ONE, 2013; 8 (2): e52970 DOI: 10.1371/journal.pone.0052970)

Dr. Darren Schreiber, a researcher in neuropolitics at the University of Exeter, has been working in collaboration with colleagues at the University of California, San Diego on research that explores the differences in the way the brain functions in American liberals and conservatives. The findings are published Feb. 13 in the journalPLOS ONE.

In a prior experiment, participants had their brain activity measured as they played a simple gambling game. Dr. Schreiber and his UC San Diego collaborators were able to look up the political party registration of the participants in public records. Using this new analysis of 82 people who performed the gambling task, the academics showed that Republicans and Democrats do not differ in the risks they take. However, there were striking differences in the participants’ brain activity during the risk-taking task.

Democrats showed significantly greater activity in the left insula, a region associated with social and self-awareness. Meanwhile Republicans showed significantly greater activity in the right amygdala, a region involved in the body’s fight-or-flight system. These results suggest that liberals and conservatives engage different cognitive processes when they think about risk.

In fact, brain activity in these two regions alone can be used to predict whether a person is a Democrat or Republican with 82.9% accuracy. By comparison, the longstanding traditional model in political science, which uses the party affiliation of a person’s mother and father to predict the child’s affiliation, is only accurate about 69.5% of the time. And another model based on the differences in brain structure distinguishes liberals from conservatives with only 71.6% accuracy.

The model also outperforms models based on differences in genes. Dr. Schreiber said: “Although genetics have been shown to contribute to differences in political ideology and strength of party politics, the portion of variation in political affiliation explained by activity in the amygdala and insula is significantly larger, suggesting that affiliating with a political party and engaging in a partisan environment may alter the brain, above and beyond the effect of heredity.”

These results may pave the way for new research on voter behaviour, yielding better understanding of the differences in how liberals and conservatives think. According to Dr. Schreiber: “The ability to accurately predict party politics using only brain activity while gambling suggests that investigating basic neural differences between voters may provide us with more powerful insights than the traditional tools of political science.”

Journal Reference:

  1. Darren Schreiber, Greg Fonzo, Alan N. Simmons, Christopher T. Dawes, Taru Flagan, James H. Fowler, Martin P. Paulus. Red Brain, Blue Brain: Evaluative Processes Differ in Democrats and RepublicansPLoS ONE, 2013; 8 (2): e52970 DOI:10.1371/journal.pone.0052970

Neuroscientists Pinpoint Location of Fear Memory in Amygdala (Science Daily)

Jan. 27, 2013 — A rustle of undergrowth in the outback: it’s a sound that might make an animal or person stop sharply and be still, in the anticipation of a predator. That “freezing” is part of the fear response, a reaction to a stimulus in the environment and part of the brain’s determination of whether to be afraid of it.

An image showing neurons in the lateral subdivision of the central amygdala (CeL). In red are somatostain-positive (SOM+) neurons, which control fear; in green are another set of neurons known as PKC-delta cells. (Credit: Image courtesy of Bo Li)

A neuroscience group at Cold Spring Harbor Laboratory (CSHL) led by Assistant Professor Bo Li Ph.D., together with collaborator Professor Z. Josh Huang Ph.D., have just released the results of a new study that examines the how fear responses are learned, controlled, and memorized. They show that a particular class of neurons in a subdivision of the amygdala plays an active role in these processes.

Locating fear memory in the amygdala

Previous research had indicated that structures inside the amygdalae, a pair of almond-shaped formations that sit deep within the brain and are known to be involved in emotion and reward-based behavior, may be part of the circuit that controls fear learning and memory. In particular, a region called the central amygdala, or CeA, was thought to be a passive relay for the signals relayed within this circuit.

Li’s lab became interested when they observed that neurons in a region of the central amygdala called the lateral subdivision, or CeL, “lit up” in a particular strain of mice while studying this circuit.

“Neuroscientists believed that changes in the strength of the connections onto neurons in the central amygdala must occur for fear memory to be encoded,” Li says, “but nobody had been able to actually show this.”

This led the team to further probe into the role of these neurons in fear responses and furthermore to ask the question: If the central amygdala stores fear memory, how is that memory trace read out and translated into fear responses?

To examine the behavior of mice undergoing a fear test the team first trained them to respond in a Pavlovian manner to an auditory cue. The mice began to “freeze,” a very common fear response, whenever they heard one of the sounds they had been trained to fear.

To study the particular neurons involved, and to understand them in relation to the fear-inducing auditory cue, the CSHL team used a variety of methods. One of these involved delivering a gene that encodes for a light-sensitive protein into the particular neurons Li’s group wanted to look at.

By implanting a very thin fiber-optic cable directly into the area containing the photosensitive neurons, the team was able to shine colored laser light with pinpoint accuracy onto the cells, and in this manner activate them. This is a technique known as optogenetics. Any changes in the behavior of the mice in response to the laser were then monitored.

A subset of neurons in the central amygdala controls fear expression

The ability to probe genetically defined groups of neurons was vital because there are two sets of neurons important in fear-learning and memory processes. The difference between them, the team learned, was in their release of message-carrying neurotransmitters into the spaces called synapses between neurons. In one subset of neurons, neurotransmitter release was enhanced; in another it was diminished. If measurements had been taken across the total cell population in the central amygdala, neurotransmitter levels from these two distinct sets of neurons would have been averaged out, and thus would not have been detected.

Li’s group found that fear conditioning induced experience-dependent changes in the release of neurotransmitters in excitatory synapses that connect with inhibitory neurons — neurons that suppress the activity of other neurons — in the central amygdala. These changes in the strength of neuronal connections are known as synaptic plasticity.

Particularly important in this process, the team discovered, were somatostatin-positive (SOM+) neurons. Somatostatin is a hormone that affects neurotransmitter release. Li and colleagues found that fear-memory formation was impaired when they prevent the activation of SOM+ neurons.

SOM+ neurons are necessary for recall of fear memories, the team also found. Indeed, the activity of these neurons alone proved sufficient to drive fear responses. Thus, instead of being a passive relay for the signals driving fear learning and responses in mice, the team’s work demonstrates that the central amygdala is an active component, and is driven by input from the lateral amygdala, to which it is connected.

“We find that the fear memory in the central amygdala can modify the circuit in a way that translates into action — or what we call the fear response,” explains Li.

In the future Li’s group will try to obtain a better understanding of how these processes may be altered in post-traumatic stress disorder (PTSD) and other disorders involving abnormal fear learning. One important goal is to develop pharmacological interventions for such disorders.

Li says more research is needed, but is hopeful that with the discovery of specific cellular markers and techniques such as optogenetics, a breakthrough can be made.

Journal Reference:

  1. Haohong Li, Mario A Penzo, Hiroki Taniguchi, Charles D Kopec, Z Josh Huang, Bo Li. Experience-dependent modification of a central amygdala fear circuitNature Neuroscience, 2013; DOI: 10.1038/nn.3322

Are Bacteria Making You Hungry? (Science Daily)

Dec. 19, 2012 — Over the last half decade, it has become increasingly clear that the normal gastrointestinal (GI) bacteria play a variety of very important roles in the biology of human and animals. Now Vic Norris of the University of Rouen, France, and coauthors propose yet another role for GI bacteria: that they exert some control over their hosts’ appetites. Their review was published online ahead of print in the Journal of Bacteriology.

Are bacteria making you hungry? Over the last half decade, it has become increasingly clear that the normal gastrointestinal (GI) bacteria play a variety of very important roles in the biology of human and animals. (Credit: © fabiomax / Fotolia)

This hypothesis is based in large part on observations of the number of roles bacteria are already known to play in host biology, as well as their relationship to the host system. “Bacteria both recognize and synthesize neuroendocrine hormones,” Norris et al. write. “This has led to the hypothesis that microbes within the gut comprise a community that forms a microbial organ interfacing with the mammalian nervous system that innervates the gastrointestinal tract.” (That nervous system innervating the GI tract is called the “enteric nervous system.” It contains roughly half a billion neurons, compared with 85 billion neurons in the central nervous system.)

“The gut microbiota respond both to both the nutrients consumed by their hosts and to the state of their hosts as signaled by various hormones,” write Norris et al. That communication presumably goes both ways: they also generate compounds that are used for signaling within the human system, “including neurotransmitters such as GABA, amino acids such as tyrosine and tryptophan — which can be converted into the mood-determining molecules, dopamine and serotonin” — and much else, says Norris.

Furthermore, it is becoming increasingly clear that gut bacteria may play a role in diseases such as cancer, metabolic syndrome, and thyroid disease, through their influence on host signaling pathways. They may even influence mood disorders, according to recent, pioneering studies, via actions on dopamine and peptides involved in appetite. The gut bacterium,Campilobacter jejuni, has been implicated in the induction of anxiety in mice, says Norris.

But do the gut flora in fact use their abilities to influence choice of food? The investigators propose a variety of experiments that could help answer this question, including epidemiological studies, and “experiments correlating the presence of particular bacterial metabolites with images of the activity of regions of the brain associated with appetite and pleasure.”

Journal Reference:

  1. V. Norris, F. Molina, A. T. Gewirtz. Hypothesis: bacteria control host appetitesJournal of Bacteriology, 2012; DOI:10.1128/JB.01384-12

Will we ever have cyborg brains? (IO9)

Will we ever have cyborg brains?

DEC 19, 2012 2:40 PM

By George Dvorsky

Over at BBC Future, computer scientist Martin Angler has put together a provocative piece about humanity’s collision course with cybernetic technologies. Today, says Angler, we’re using neural interface devices and other assistive technologies to help the disabled. But in short order we’ll be able to radically enhance human capacites — prompting him to wonder about the extent to which we might cyborgize our brains.

Angler points to two a recent and equally remarkable breakthroughs, including a paralyzed stroke victim who was able to guide a robot arm that delivered a hot drink, and a thought-controlled prosthetic hand that could grasp a variety of objects.

Admitting that it’s still early days, Angler speculates about the future:

Yet it’s still a far cry from the visions of man fused with machine, or cyborgs, that grace computer games or sci-fi. The dream is to create the type of brain augmentations we see in fiction that provide cyborgs with advantages or superhuman powers. But the ones being made in the lab only aim to restore lost functionality – whether it’s brain implants that restore limb control, or cochlear implants for hearing.

Creating implants that improve cognitive capabilities, such as an enhanced vision “gadget” that can be taken from a shelf and plugged into our brain, or implants that can restore or enhance brain function is understandably a much tougher task. But some research groups are being to make some inroads.

For instance, neuroscientists Matti Mintz from Tel Aviv University and Paul Verschure from Universitat Pompeu Fabra in Barcelona, Spain, are trying to develop an implantable chip that can restore lost movement through the ability to learn new motor functions, rather than regaining limb control. Verschure’s team has developed a mathematical model that mimics the flow of signals in the cerebellum, the region of the brain that plays an important role in movement control. The researchers programmed this model onto a circuit and connected it with electrodes to a rat’s brain. If they tried to teach the rat a conditioned motor reflex – to blink its eye when it sensed an air puff – while its cerebellum was “switched off” by being anaesthetised, it couldn’t respond. But when the team switched the chip on, this recorded the signal from the air puff, processed it, and sent electrical impulses to the rat’s motor neurons. The rat blinked, and the effect lasted even after it woke up.

Be sure to read the entire article, as Angler discusses uplifted monkeys, the tricky line that divides a human brain from a cybernetic one, and the all-important question of access.

Image: BBC/Science Photo Library.

Brazilian Mediums Shed Light On Brain Activity During a Trance State (Science Daily)

ScienceDaily (Nov. 16, 2012) — Researchers at Thomas Jefferson University and the University of Sao Paulo in Brazil analyzed the cerebral blood flow (CBF) of Brazilian mediums during the practice of psychography, described as a form of writing whereby a deceased person or spirit is believed to write through the medium’s hand. The new research revealed intriguing findings of decreased brain activity during the mediums’ dissociative state which generated complex written content. Their findings will appear in the November 16th edition of the online journal PLOS ONE.

The 10 mediums — five less expert and five experienced — were injected with a radioactive tracer to capture their brain activity during normal writing and during the practice of psychography which involves the subject entering a trance-like state. The subjects were scanned using SPECT (single photon emission computed tomography) to highlight the areas of the brain that are active and inactive during the practice.

“Spiritual experiences affect cerebral activity, this is known. But, the cerebral response to mediumship, the practice of supposedly being in communication with, or under the control of the spirit of a deceased person, has received little scientific attention, and from now on new studies should be conducted,” says Andrew Newberg, MD, director of Research at the Jefferson-Myrna Brind Center of Integrative Medicine and a nationally-known expert on spirituality and the brain, who collaborated with Julio F. P. Peres, Clinical Psychologist, PhD in Neuroscience and Behavior, Institute of Psychology at the University of Sao Paulo in Brazil, and colleagues on the research.

The mediums ranged from 15 to 47 years of automatic writing experience, performing up to 18 psychographies per month. All were right-handed, in good mental health, and not currently using any psychiatric drugs. All reported that during the study, they were able to reach their usual trance-like state during the psychography task and were in their regular state of consciousness during the control task.

The researchers found that the experienced psychographers showed lower levels of activity in the left hippocampus (limbic system), right superior temporal gyrus, and the frontal lobe regions of the left anterior cingulate and right precentral gyrus during psychography compared to their normal (non-trance) writing. The frontal lobe areas are associated with reasoning, planning, generating language, movement, and problem solving, perhaps reflecting an absence of focus, self-awareness and consciousness during psychography, the researchers hypothesize.

Less expert psychographers showed just the opposite — increased levels of CBF in the same frontal areas during psychography compared to normal writing. The difference was significant compared to the experienced mediums. This finding may be related to their more purposeful attempt at performing the psychography. The absence of current mental disorders in the groups is in line with current evidence that dissociative experiences are common in the general population and not necessarily related to mental disorders, especially in religious/spiritual groups. Further research should address criteria for distinguishing between healthy and pathological dissociative expressions in the scope of mediumship.

The writing samples produced were also analyzed and it was found that the complexity scores for the psychographed content were higher than those for the control writing across the board. In particular, the more experienced mediums showed higher complexity scores, which typically would require more activity in the frontal and temporal lobes, but this was not the case. Content produced during psychographies involved ethical principles, the importance of spirituality, and bringing together science and spirituality.

Several possible hypotheses for these many differences have been considered. One speculation is that as frontal lobe activity decreases, the areas of the brain that support mediumistic writing are further disinhibited (similar to alcohol or drug use) so that the overall complexity can increase. In a similar manner, improvisational music performance is associated with lower levels of frontal lobe activity which allows for more creative activity. However, improvisational music performance and alcohol/drug consumption states are quite peculiar and distinct from psychography. “While the exact reason is at this point elusive, our study suggests there are neurophysiological correlates of this state,” says Newberg.

“This first-ever neuroscientific evaluation of mediumistic trance states reveals some exciting data to improve our understanding of the mind and its relationship with the brain. These findings deserve further investigation both in terms of replication and explanatory hypotheses,” states Newberg.

Journal Reference:

  1. Julio Fernando Peres, Alexander Moreira-Almeida, Leonardo Caixeta, Frederico Leao, Andrew Newberg. Neuroimaging during Trance State: A Contribution to the Study of DissociationPLoS ONE, 2012; 7 (11): e49360 DOI:10.1371/journal.pone.0049360

Books Change How a Child’s Brain Grows (Wired)

By Moheb Costandi, ScienceNOW – October 18, 2012

Image: Peter Dedina/Flickr

NEW ORLEANS, LOUISIANA — Books and educational toys can make a child smarter, but they also influence how the brain grows, according to new research presented here on Sunday at the annual meeting of the Society for Neuroscience. The findings point to a “sensitive period” early in life during which the developing brain is strongly influenced by environmental factors.

Studies comparing identical and nonidentical twins show that genes play an important role in the development of the cerebral cortex, the thin, folded structure that supports higher mental functions. But less is known about how early life experiences influence how the cortex grows.

To investigate, neuroscientist Martha Farah of the University of Pennsylvania and her colleagues recruited 64 children from a low-income background and followed them from birth through to late adolescence. They visited the children’s homes at 4 and 8 years of age to evaluate their environment, noting factors such as the number of books and educational toys in their houses, and how much warmth and support they received from their parents.

More than 10 years after the second home visit, the researchers used MRI to obtain detailed images of the participants’ brains. They found that the level of mental stimulation a child receives in the home at age 4 predicted the thickness of two regions of the cortex in late adolescence, such that more stimulation was associated with a thinner cortex. One region, the lateral inferior temporal gyrus, is involved in complex visual skills such as word recognition.

Home environment at age 8 had a smaller impact on development of these brain regions, whereas other factors, such as the mother’s intelligence and the degree and quality of her care, had no such effect.

Previous work has shown that adverse experiences, such as childhood neglect, abuse, and poverty, can stunt the growth of the brain. The new findings highlight the sensitivity of the growing brain to environmental factors, Farah says, and provide strong evidence that subtle variations in early life experience can affect the brain throughout life.

As the brain develops, it produces more synapses, or neuronal connections, than are needed, she explains. Underused connections are later eliminated, and this elimination process, called synaptic pruning, is highly dependent upon experience. The findings suggest that mental stimulation in early life increases the extent to which synaptic pruning occurs in the lateral temporal lobe. Synaptic pruning reduces the volume of tissue in the cortex. This makes the cortex thinner, but it also makes information processing more efficient.

“This is a first look at how nurture influences brain structure later in life,” Farah reported at the meeting. “As with all observational studies, we can’t really speak about causality, but it seems likely that cognitive stimulation experienced early in life led to changes in cortical thickness.”

She adds, however, that the research is still in its infancy, and that more work is needed to gain a better understanding of exactly how early life experiences impact brain structure and function.

The findings add to the growing body of evidence that early life is a period of “extreme vulnerability,” says psychiatrist Jay Giedd, head of the brain imaging unit in the Child Psychiatry Branch at the National Institute of Mental Health in Bethesda, Maryland. But early life, he says, also offers a window of opportunity during which the effects of adversity can be offset. Parents can help young children develop their cognitive skills by providing a stimulating environment.

Evolution mostly driven by brawn, not brains (University College London)

Public release date: 15-Oct-2012
By Clare Ryan
University College London

The most common measure of intelligence in animals, brain size relative to body size, may not be as dependent on evolutionary selection on the brain as previously thought, according to a new analysis by scientists.

Brain size relative to body size has been used by generations of scientists to predict an animal’s intelligence. For example, although the human brain is not the largest in the animal kingdom in terms of volume or mass, it is exceptionally large considering our moderate body mass.

Now, a study by a team of scientists at UCL, the University of Konstanz, and the Max Planck Institute of Ornithology has found that the relationship between the two traits is driven by different evolutionary mechanisms in different animals.

Crucially, researchers have found that the most significant factor in determining relative brain size is often evolutionary pressure on body size, and not brain size. For example, the evolutionary history of bats reveals they decreased body size much faster than brain size, leading to an increase in relative brain size. As a result, small bats were able to evolve improved flying manoeuvrability while maintaining the brainpower to handle foraging in cluttered environments.

This shows that relative brain size can not be used unequivocally as evidence of selection for intelligence. The study is published today in the Proceedings of the National Academy of Sciences.

Dr Jeroen Smaers (UCL Anthropology and UCL Genetics, Evolution & Environment), lead author of the study said: “When using brain size relative to body size as a measure of intelligence, the assumption has always been that this measure is primarily driven by changes in brain size. It now appears that the relationship between changes in brain and body size in animals is more complex than has long been assumed.

“Changes in body size often occur independently of changes in brain size and vice versa. Moreover, the nature of these independent changes in brain and body size, are different in different groups of animals.”

Researchers at UCL gathered data on brain and body mass for hundreds of modern and extinct bats, carnivorans, and primates. They then charted brain and body size evolution over time for each species. Across millions of years, most animals increased body size faster than brain size, with the exception of bats.

In primate lineages decreases in brain size marginally outpaced those in body size. Carnivoran evolution has taken yet a different course, with changes generally more strongly associated with body size rather than selection on brain size and cognition.

Given such differences, the authors believe that the predominant interpretation of relative brain size as the consequence of selection on intelligence inherently masks the often more significant influence of selection on body size.

Mathematics or Memory? Study Charts Collision Course in Brain (Science Daily)

ScienceDaily (Sep. 3, 2012) — You already know it’s hard to balance your checkbook while simultaneously reflecting on your past. Now, investigators at the Stanford University School of Medicine — having done the equivalent of wire-tapping a hard-to-reach region of the brain — can tell us how this impasse arises.

The area in red is the posterior medial cortex, the portion of the brain that is most active when people recall details of their own pasts. (Credit: Courtesy of Josef Parvizi)

The researchers showed that groups of nerve cells in a structure called the posterior medial cortex, or PMC, are strongly activated during a recall task such as trying to remember whether you had coffee yesterday, but just as strongly suppressed when you’re engaged in solving a math problem.

The PMC, situated roughly where the brain’s two hemispheres meet, is of great interest to neuroscientists because of its central role in introspective activities.

“This brain region is famously well-connected with many other regions that are important for higher cognitive functions,” said Josef Parvizi, MD, PhD, associate professor of neurology and neurological sciences and director of Stanford’s Human Intracranial Cognitive Electrophysiology Program. “But it’s very hard to reach. It’s so deep in the brain that the most commonly used electrophysiological methods can’t access it.”

In a study published online Sept. 3 in Proceedings of the National Academy of Sciences, Parvizi and his Stanford colleagues found a way to directly and sensitively record the output from this ordinarily anatomically inaccessible site in human subjects. By doing so, the researchers learned that particular clusters of nerve cells in the PMC that are most active when you are recalling details of your own past are strongly suppressed when you are performing mathematical calculations. Parvizi is the study’s senior author. The first and second authors, respectively, are postdoctoral scholars Brett Foster, PhD, and Mohammed Dastjerdi, PhD.

Much of our understanding of what roles different parts of the brain play has been obtained by techniques such as functional magnetic resonance imaging, which measures the amount of blood flowing through various brain regions as a proxy for activity in those regions. But changes in blood flow are relatively slow, making fMRI a poor medium for listening in on the high-frequency electrical bursts (approximately 200 times per second) that best reflect nerve-cell firing. Moreover, fMRI typically requires pooling images from several subjects into one composite image. Each person’s brain physiognomy is somewhat different, so the blending blurs the observable anatomical coordinates of a region of interest.

Nonetheless, fMRI imaging has shown that the PMC is quite active in introspective processes such as autobiographical memory processing (“I ate breakfast this morning”) or daydreaming, and less so in external sensory processing (“How far away is that pedestrian?”). “Whenever you pay attention to the outside world, its activity decreases,” said Parvizi.

To learn what specific parts of this region are doing during, say, recall versus arithmetic requires more-individualized anatomical resolution than an fMRI provides. Otherwise, Parvizi said, “if some nerve-cell populations become less active and others more active, it all washes out, and you see no net change.” So you miss what’s really going on.

For this study, the Stanford scientists employed a highly sensitive technique to demonstrate that introspective and externally focused cognitive tasks directly interfere with one another, because they impose opposite requirements on the same brain circuitry.

The researchers took advantage of a procedure performed on patients who were being evaluated for brain surgery at the Stanford Epilepsy Monitoring Unit, associated with Stanford University Medical Center. These patients were unresponsive to drug therapy and, as a result, suffered continuing seizures. The procedure involves temporarily removing small sections of a patient’s skull, placing a thin plastic film containing electrodes onto the surface of the brain near the suspected point of origin of that patient’s seizure (the location is unique to each patient), and then monitoring electrical activity in that region for five to seven days — all of it spent in a hospital bed. Once the epilepsy team identifies the point of origin of any seizures that occurred during that time, surgeons can precisely excise a small piece of tissue at that position, effectively breaking the vicious cycle of brain-wave amplification that is a seizure.

Implanting these electrode packets doesn’t mean piercing the brain or individual cells within it. “Each electrode picks up activity from about a half-million nerve cells,” Parvizi said. “It’s more like dotting the ceiling of a big room, filled with a lot of people talking, with multiple microphones. We’re listening to the buzz in the room, not individual conversations. Each microphone picks up the buzz from a different bunch of partiers. Some groups are more excited and talking more loudly than others.”

The experimenters found eight patients whose seizures were believed to be originating somewhere near the brain’s midline and who, therefore, had had electrode packets placed in the crevasse dividing the hemispheres. (The brain’s two hemispheres are spaced far enough apart to slip an electrode packet between them without incurring damage.)

The researchers got permission from these eight patients to bring in laptop computers and put the volunteers through a battery of simple tasks requiring modest intellectual effort. “It can be boring to lie in bed waiting seven days for a seizure to come,” said Foster. “Our studies helped them pass the time.” The sessions lasted about an hour.

On the laptop would appear a series of true/false statements falling into one of four categories. Three categories were self-referential, albeit with varying degrees of specificity. Most specific was so-called “autobiographical episodic memory,” an example of which might be: “I drank coffee yesterday.” The next category of statements was more generic: “I eat a lot of fruit.” The most abstract category, “self-judgment,” comprised sentences along the lines of: “I am honest.”

A fourth category differed from the first three in that it consisted of arithmetical equations such as: 67 + 6 = 75. Evaluating such a statement’s truth required no introspection but, instead, an outward, more sensory orientation.

For each item, patients were instructed to press “1” if a statement was true, “2” if it was false.

Significant portions of the PMC that were “tapped” by electrodes became activated during self-episodic memory processing, confirming the PMC’s strong role in recall of one’s past experiences. Interestingly, true/false statements involving less specifically narrative recall — such as, “I eat a lot of fruit” — induced relatively little activity. “Self-judgment” statements — such as, “I am attractive” — elicited none at all. Moreover, whether a volunteer judged a statement to be true or false made no difference with respect to the intensity, location or duration of electrical activity in activated PMC circuits.

This suggests, both Parvizi and Foster said, that the PMC is not the brain’s “center of self-consciousness” as some have proposed, but is more specifically engaged in constructing autobiographical narrative scenes, as occurs in recall or imagination.

Foster, Dastjerdi and Parvizi also found that the PMC circuitry activated by a recall task took close to a half-second to fire up, ruling out the possibility that this circuitry’s true role was in reading or making sense of the sentence on the screen. (These two activities are typically completed within the first one-fifth of a second or so.) Once activated, these circuits remained active for a full second.

Yet all the electrodes that lit up during the self-episodic condition were conspicuously deactivated during arithmetic calculation. In fact, the circuits being monitored by these electrodes were not merely passively silent, but actively suppressed, said Parvizi. “The more a circuit is activated during autobiographical recall, the more it is suppressed during math. It’s essentially impossible to do both at once.”

The study was funded by the National Institutes of Health, with partial sponsorship from the Stanford Institute for NeuroInnovation and Translational Neuroscience.