Posts tagged psychology

March 23, 2012 by Cathryn Delude

Our fond or fearful memories — that first kiss or a bump in the night — leave memory traces that we may conjure up in the remembrance of things past, complete with time, place and all the sensations of the experience. Neuroscientists call these traces memory engrams.

But are engrams conceptual, or are they a physical network of neurons in the brain? In a new MIT study, researchers used optogenetics to show that memories really do reside in very specific brain cells, and that simply activating a tiny fraction of brain cells can recall an entire memory — explaining, for example, how Marcel Proust could recapitulate his childhood from the aroma of a once-beloved madeleine cookie.

“We demonstrate that behavior based on high-level cognition, such as the expression of a specific memory, can be generated in a mammal by highly specific physical activation of a specific small subpopulation of brain cells, in this case by light,” says Susumu Tonegawa, the Picower Professor of Biology and Neuroscience at MIT and lead author of the study reported online today in the journal Nature. “This is the rigorously designed 21st-century test of Canadian neurosurgeon Wilder Penfield’s early-1900s accidental observation suggesting that mind is based on matter.”

In that famous surgery, Penfield treated epilepsy patients by scooping out parts of the brain where seizures originated. To ensure that he destroyed only the problematic neurons, Penfield stimulated the brain with tiny jolts of electricity while patients, who were under local anesthesia, reported what they were experiencing. Remarkably, some vividly recalled entire complex events when Penfield stimulated just a few neurons in the hippocampus, a region now considered essential to the formation and recall of episodic memories.

Scientists have continued to explore that phenomenon but, until now, it has never been proven that the direct reactivation of the hippocampus was sufficient to cause memory recall.

Shedding light on the matter

Fast forward to the introduction, seven years ago, of optogenetics, which can stimulate neurons that are genetically modified to express light-activated proteins. “We thought we could use this new technology to directly test the hypothesis about memory encoding and storage in a mimicry experiment,” says co-author Xu Liu, a postdoc in Tonegawa’s lab. 

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ScienceDaily (Mar. 23, 2012) — Insulin resistance in the brain precedes and contributes to cognitive decline above and beyond other known causes of Alzheimer’s disease, according to a new study by researchers from the Perelman School of Medicine at the University of Pennsylvania. Insulin is an important hormone in many bodily functions, including the health of brain cells. The team identified extensive abnormalities in the activity of two major signaling pathways for insulin and insulin-like growth factor in non-diabetic people with Alzheimer’s disease. These pathways could be targeted with new or existing medicines to potentially help resensitize the brain to insulin and possibly slow down or even improve cognitive decline.

This is the first study to directly demonstrate that insulin resistance occurs in the brains of people with Alzheimer’s disease. The study is now online in the Journal of Clinical Investigation.

"Our research clearly shows that the brain’s ability to respond to insulin, which is important for normal brain function, is going offline at some point. Insulin in the brain not only modulates glucose uptake, but also promotes the health of brain cells — their growth, survival, remodeling, and normal functioning. We believe that brain insulin resistance may be an important contributor to the cognitive decline associated with Alzheimer’s disease," said senior author, Steven E. Arnold, MD, professor of Psychiatry and Neurology. Arnold is also the director of the Penn Memory Center, a National Institute on Aging-designated Alzheimer’s Disease Core Center. "If we can prevent brain insulin resistance from occurring, or re-sensitize brain cells to insulin with any of the currently available insulin-sensitizing diabetes medicines, we may be able to slow down, prevent, or perhaps even improve cognitive decline.

The risk of developing Alzheimer’s disease is increased by 50 percent in people with diabetes. Type 2 diabetes is due to insulin resistance and accounts for 90 percent of all diabetes. The defining clinical feature of Type 2 diabetes (and Type 1 “juvenile” diabetes) is hyperglycemia — high levels of sugar in the blood — but there is no evidence that the brain in Alzheimer’s is hyperglycemic. Insulin acts differently in the brain than in the rest of the body. Researchers found that insulin resistance of the brain occurs in Alzheimer’s disease independent of whether someone has diabetes, by excluding people with a history of diabetes from this study.

The investigators used samples of postmortem brain tissue from non-diabetics who had died with Alzheimer’s disease, stimulated the tissue with insulin, and measured how much the insulin activated various proteins in the insulin-signaling pathways. There was less insulin activation in Alzheimer’s cases than in tissue from people who had died without brain disease. Other proteins linked to insulin action in the brain were abnormal in Alzheimer’s disease samples. These abnormalities were highly correlated with episodic memory and other cognitive disabilities in the Alzheimer’s disease patients.

In tissue from people with Alzheimer’s disease and mild cognitive impairment (MCI), researchers found that changes to a protein called insulin receptor substrate-1 (IRS-1 pS636/639 and pS616) in brain cells were linked to the severity of memory impairments regardless of age, sex, diabetes history, or apolipoprotein E (APOE) gene status. Levels of IRS-1 were also significantly associated with, but not likely to affect, the presence of amyloid beta plaques and neurofibrillary tangles, the signature markers of Alzheimer’s disease. This suggests that insulin resistance contributes to cognitive decline independent of the classical pathology of Alzheimer’s disease.

Researchers noted that three insulin-sensitizing medicines are already approved by the FDA for treatment of diabetes. These drugs readily cross the blood-brain barrier and may have therapeutic potential to correct insulin resistance in Alzheimer’s disease and MCI. “Clinical trials would need to be conducted to determine the impact the drugs have on Alzheimer’s disease and MCI in non-diabetic patients,” said Dr. Arnold.

Source: Science Daily

March 23, 2012

One cup or two faces? What we believe we see in one of the most famous optical illusions changes in a split second; and so does the path that the information takes in the brain. In a new theoretical study, scientists of the Max Planck Institute for Dynamics and Self-Organization, the Bernstein Center Göttingen and the German Primate Center now show how this is possible without changing the cellular links of the network. The direction of information flow changes, depending on the time pattern of communication between brain areas. This reorganisation can be triggered even by a slight stimulus, such as a scent or sound, at the right time.

The way how the different regions of the brain are connected with each other plays a significant role for information processing. This processing can be changed by the assembling and disassembling of nerve fibres joining distant brain circuits. But such events are much too slow to explain rapid changes in perception. From experimental studies it was known that the responsible actions must be at least two orders of magnitude faster. The Göttingen scientists now show for the first time that it is possible to change the information flow in a tightly interconnected network in a simple manner.

Many areas of the brain display a rhythmic nerve cell activity. “The interacting brain areas are like metronomes that tick at the same speed and in a distinct temporal pattern,” says the physicist and principal investigator Demian Battaglia. The researchers were now able to demonstrate that this temporal pattern determines the information flow. “If one of the metronomes is affected, e.g. through an external stimulus, then it changes beat, ticking in an altered temporal pattern compared to the others. The other areas adapt to this new situation through self-organisation and start playing a different drum beat as well. It is therefore sufficient to impact one of the areas in the network to completely reorganize its functioning, as we have shown in our model,” explains Battaglia.

The applied perturbation does not have to be particularly strong. “It is more important that the ‘kick’ occurs at exactly the right time of the rhythm,” says Battaglia. This might play a significant role for perception processes: “When viewing a picture, we are trained to recognize faces as quickly as possible – even if there aren’t any,” points out the Göttingen researcher. “But if we smell a fragrance reminiscent of wine, we immediately see the cup in the picture. This allows us to quickly adjust to things that we did not expect, changing the focus of our attention.”

Next, the scientists want to test the model on networks with a more realistic anatomy. They also hope that the findings inspire future experimental studies, as Battaglia says: “It would be fantastic if, in some years, certain brain areas could be stimulated so finely and precisely that the theoretically predicted effects can be measured through imaging methods.”

Provided by Max-Planck-Gesellschaft

Source: medicalxpress.com

ScienceDaily (Mar. 22, 2012) — Anxious people have a heightened sense of smell when it comes to sniffing out a threat, according to a new study by Elizabeth Krusemark and Wen Li from the University of Wisconsin-Madison in the US.

In animals, the sense of smell is an essential tool to detect, locate and identify predators in the surrounding environment. In fact, the olfactory-mediated defense system is so prominent in animals, that the mere presence of predator odors can evoke potent fear and anxiety responses.

Smells also evoke powerful emotional responses in humans. Krusemark and Li hypothesized that in humans, detection of a particular bad smell may signal danger of a noxious airborne substance, or a decaying object that carries disease.

Their work is published online in Springer’s journal Chemosensory Perception. The study is part of a special issue of this journal on neuroimaging the chemical senses.

The researchers exposed 14 young adult participants to three types of odors: neutral pure odor, neutral odor mixture, and negative odor mixture. They asked them to detect the presence or absence of an odor in an MRI scanner. During scanning, the researchers also measured the skin’s ability to conduct electricity (a measure of arousal level) and monitored the subjects’ breathing patterns. Once the odor detection task was over, and the subjects were still in the scanner, they were asked to rate their current level of anxiety. The authors then analyzed the brain images obtained.

They found that as anxiety levels rose, so did the subjects’ ability to discriminate negative odors accurately — suggesting a ‘remarkable’ olfactory acuity to threat in anxious subjects. The skin conductance results showed that anxiety also heightened emotional arousal to smell-induced threats.

The authors uncovered amplified communication between the sensory and emotional areas of the brain in response to negative odors, particularly in anxiety. This increased connectivity could be responsible for the heightened arousal to threats.

Krusemark and Li conclude: “This enhanced sensory-emotional coupling could serve as a critical mechanism to arouse adequate physiological alertness to potential insults.”

Source: Science Daily

March 22, 2012

Scripps Research Institute scientists and their colleagues have successfully harnessed neurons in mouse brains, allowing them to at least partially control a specific memory. Though just an initial step, the researchers hope such work will eventually lead to better understanding of how memories form in the brain, and possibly even to ways to weaken harmful thoughts for those with conditions such as schizophrenia and post traumatic stress disorder.

The results are reported in the March 23, 2012 issue of the journal Science.

Researchers have known for decades that stimulating various regions of the brain can trigger behaviors and even memories. But understanding the way these brain functions develop and occur normally—effectively how we become who we are—has been a much more complex goal.

"The question we’re ultimately interested in is: How does the activity of the brain represent the world?" said Scripps Research neuroscientist Mark Mayford, who led the new study. "Understanding all this will help us understand what goes wrong in situations where you have inappropriate perceptions. It can also tell us where the brain changes with learning."

On-Off Switches and a Hybrid Memory

As a first step toward that end, the team set out to manipulate specific memories by inserting two genes into mice. One gene produces receptors that researchers can chemically trigger to activate a neuron. They tied this gene to a natural gene that turns on only in active neurons, such as those involved in a particular memory as it forms, or as the memory is recalled. In other words, this technique allows the researchers to install on-off switches on only the neurons involved in the formation of specific memories.

For the study’s main experiment, the team triggered the “on” switch in neurons active as mice were learning about a new environment, Box A, with distinct colors, smells and textures.

Next the team placed the mice in a second distinct environment—Box B—after giving them the chemical that would turn on the neurons associated with the memory for Box A. The researchers found the mice behaved as if they were forming a sort of hybrid memory that was part Box A and part Box B. The chemical switch needed to be turned on while the mice were in Box B for them to demonstrate signs of recognition. Alone neither being in Box B nor the chemical switch was effective in producing memory recall.

"We know from studies in both animals and humans that memories are not formed in isolation but are built up over years incorporating previously learned information," Mayford said. "This study suggests that one way the brain performs this feat is to use the activity pattern of nerve cells from old memories and merge this with the activity produced during a new learning session."

Future Manipulation of the Past

The team is now making progress toward more precise control that will allow the scientists to turn one memory on and off at will so effectively that a mouse will in fact perceive itself to be in Box A when it’s in Box B.

Once the processes are better understood, Mayford has ideas about how researchers might eventually target the perception process through drug treatment to deal with certain mental diseases such as schizophrenia and post traumatic stress disorder. With such problems, patients’ brains are producing false perceptions or disabling fears. But drug treatments might target the neurons involved when a patient thinks about such fear, to turn off the neurons involved and interfere with the disruptive thought patterns.

Provided by The Scripps Research Institute

Source: medicalxpress.com

ScienceDaily (Mar. 21, 2012) — Scientists at the Stanford University School of Medicine have shown for the first time how brain function differs in people who have math anxiety from those who don’t.

A series of scans conducted while second- and third-grade students did addition and subtraction revealed that those who feel panicky about doing math had increased activity in brain regions associated with fear, which caused decreased activity in parts of the brain involved in problem-solving.

"The same part of the brain that responds to fearful situations, such as seeing a spider or snake, also shows a heightened response in children with high math anxiety," said Vinod Menon, PhD, the Stanford professor of psychiatry and behavioral sciences who led the research.

In their new study, published online March 20 in Psychological Science, a journal of the Association for Psychological Science, Menon’s team performed functional magnetic resonance imaging brain scans on 46 second- and third-grade students with low and high math anxiety. Outside the fMRI scanner, the children were assessed for math anxiety with a modified version of a standardized questionnaire for adults, and also received standard intelligence and cognitive tests.

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ScienceDaily (Mar. 21, 2012) — Healthy individuals who carry a gene variation linked to an increased risk of autism have structural differences in their brains that may help explain how the gene affects brain function and increases vulnerability for autism. The results of this innovative brain imaging study are described in an article in the groundbreaking neuroscience journal Brain Connectivity, a bimonthly peer-reviewed publication from Mary Ann Liebert, Inc. The article is available free online at the Brain Connectivity website.

"This is one of the first papers demonstrating a linkage between a particular gene variant and changes in brain structure and connectivity in carriers of that gene," says Christopher Pawela, PhD, Co-Editor-in-Chief and Assistant Professor, Medical College of Wisconsin. "This work could lead to the creation of an exciting new line of research investigating the impact of genetics on communication between brain regions."

Although carriers of the common gene variant CNTNAP2 — identified as an autism risk gene — may not develop autism, there is evidence of differences in brain structure that may affect connections and signaling between brain regions. These disruptions in brain connectivity can give rise to functional abnormalities characteristic of neuropsychological disorders such as autism.

Emily Larson Dennis, Neda Jahanshad, Jeffrey D Rudie, Jesse A Brown, Kori Johnson, Katie McMahon, Greig de Zubicaray, Grant Montgomery, Nicholas Martin, Margaret Wright, Susan Bookheimer, Mirella Dapretto, Arthur Toga, Paul Thompson. Altered Structural Brain Connectivity in Healthy Carriers of the Autism Risk Gene, CNTNAP2. Brain Connectivity, 2012; 120229030236004 DOI: 10.1089/brain.2011.0064

Source: Science Daily

ScienceDaily (Mar. 21, 2012) — Why does inhaling anesthetics cause unconsciousness? New insights into this century-and-a-half-old question may spring from research performed at the National Institute of Standards and Technology (NIST). Scientists from NIST and the National Institutes of Health have found hints that anesthesia may affect the organization of fat molecules, or lipids, in a cell’s outer membrane — potentially altering the ability to send signals along nerve cell membranes.

"A better fundamental understanding of inhaled anesthetics could allow us to design better ones with fewer side effects," says Hirsh Nanda, a scientist at the NIST Center for Neutron Research (NCNR). "How these chemicals work in the body is a scientific mystery that stretches back to the Civil War."

At the turn of the 20th century, doctors suspected inhaled anesthetics had some effect on cell membranes, an animal cell’s outer boundary. Despite considerable investigation, however, no one was able to demonstrate that anesthetics produced changes in the physical properties of membranes large enough to cause anesthesia. But eventually, understanding of membrane function grew more refined as scientists learned more about ion channels.

Ion channels — large proteins embedded in the relatively small lipid molecules forming the membrane — are responsible for conducting electrical impulses along nerve cells in the brain and throughout our body. By a few decades ago, the prevailing theory held that inhaled anesthetics directly interacted with these protein channels, affecting their behavior in some fashion. But no one could find a single type of ion channel that reacted to anesthetics in a way pivotal enough to settle the matter, and the question remained open.

"That’s where we picked up the thread," says Nanda. "We had been looking at how different types of lipid molecules affect ion channels."

While a cell membrane is a highly fluid film made of many different kinds of lipid molecules, the region immediately surrounding an ion channel often consists of a single type of lipids that form a sort of “raft” that is more ordered and less fluid then the rest of the membrane. When the team heard other researchers had found that disrupting these lipid rafts could affect a channel’s function, they put to work their own previous experience working with the channels.

"We decided to test whether inhaled anesthetics could have an effect on rafts in model cell membranes," Nanda says. "No one had thought to ask the question before."

Using the NCNR’s neutron and X-ray diffraction devices as their microscope, the team explored how a model cell membrane responded to two chemicals — inhaled anesthetic, and another that has many of the same chemical properties as anesthetic but does not cause unconsciousness. Their finding showed a distinct difference in the way the lipid rafts responded: Exposing the membranes to an anesthetic caused the rafts to grow disorderly, freely mixing its lipids with the surrounding membrane, but the second chemical had a dramatically smaller effect.

While Nanda says the discovery does not answer the question definitively, he and his co-authors are following up with other experiments that could clarify the issue. “We feel the discovery has opened up an entirely new line of inquiry into this very old puzzle,” he says.

Source: Science Daily

March 21, 2012

Scientists from Germany discovered new functions of brain regions that are responsible for seeing movement.

When observing a fly buzzing around the room, we should have the impression that it is not the fly, but rather the space that lies behind it that is moving. After all, the fly is always fixed in our central point of view. But how does the brain convey the impression of a fly in motion in a motionless field? With the help of functional magnetic resonance imaging (fMRI) scientists from the Werner Reichardt Centre for Integrative Neuroscience and the Max Planck Institute for Biological Cybernetics in Tübingen have identified two areas of the brain that compare the movements of the eye with the visual movements cast onto the retina so as to correctly perceive objects in motion.

The two areas of the brain that are particularly good at reacting to external movements, even during eye movements, are known as V3A and V6. They are located in the upper half in the posterior part of the brain. Area V3A shows a high degree of integration: it reacts to movements around us regardless of whether or not we follow the moving object with our eyes. But the area does not react to visual movements on the retina when eye movements produce them. Area V6 has similar characteristics. In addition, it can perform these functions when we are moving forwards. The calculations the brain has to perform are more complicated in this case: the three-dimensional, expanding forward movement is superimposed onto the two-dimensional lateral movements that are caused by eye movements.

The scientists Elvira Fischer and Andreas Bartels from the Werner Reichardt Centre for Integrative Neuroscience and the Max Planck Institute for Biological Cybernetics have investigated these areas with the help of functional magnetic resonance imaging (fMRI). fMRI is a procedure that can measure brain activity based on local changes in blood flow and oxygen consumption. Participants in the study were shown various visual scenarios whilst undergoing fMRI scanning. For example, they had to follow a small dot with their eyes while it moved across a screen from one side to the other. The patterned background was either stationary or moved at varying speeds, sometimes slower, faster or at the same speed as the dot. Sometimes the dot was stationary while only the background moved. In a total of six experiments the scientists measured brain activity in more than a dozen different scenarios. From this they have been able to discover that V3A and V6, unlike other visual areas in the brain, have a pronounced ability to compare eye movements with the visual signals on the retina. “I am especially fascinated by V3A because it reacts so strongly and selectively to movements in our surroundings. It sounds trivial, but it is an astonishing capability of the brain”, explains Andreas Bartels, project leader of the study.

Whether it is ourselves who move or something else in our surroundings is a problem about which we seldom think, since at the subconscious level our brain constantly calculates and corrects our visual impression. Indeed, patients who have lost this ability to integrate movements in their surroundings with their eye movements can no longer recognize what it is that ultimately is moving: the surroundings or themselves. Every time they move their eyes these patients feel dizzy. Studies such as this bring us one step closer to an understanding of the causes of such illnesses.

Provided by Max-Planck-Gesellschaft

Source: medicalxpress.com

March 21, 2012

(Medical Xpress) — People who lose their sight at a later stage in life have a greater spatial awareness than if they were born blind, according to scientists at Queen Mary, University of London.

The study, published in the journal Neuroscience and Biobehavioral Reviews, examined research which looked at the spatial skills of sighted and blind people and found that some spatial tasks need visual experience.

Co-author on the study, Dr. Michael Proulx from Queen Mary’s School of Biological and Chemical Sciences, said: “Numerous studies have tested how humans use vision for knowing the spatial locations of things yet few have examined the other senses and whether people with a visual impairment use the same strategies.

“In reviewing research already available, we found visual experience is necessary for the brain to develop the ability to process multisensory information. We use vision and the other senses to create a mental map of where objects are in relation to other objects and the environment.

“Our findings suggest that there is a sensitive period during which visual experience is necessary for the brain to develop those neurons that can represent the world in this way.”

Lead author Dr. Achille Pasqualotto, also from Queen Mary’s School of Biological and Chemical Sciences, said: “Blindness reveals how well humans can function using the remaining senses, even in a world designed by sighted people for sighted people.

“The brain develops spatial abilities that relate an object’s location to the individual. This makes sense given that a visually impaired person does not see objects at a distance in an environment, but instead acquires their location by personally approaching and identifying them.”

The team is building on their findings now by testing sighted and blind people on a variety of spatial tasks that will explicitly test these findings.

They hope this research will not only reveal the psychological and neural basis for spatial cognition, but also translate into better services for blind persons, such as the development of better navigational tools.

Dr. Proulx said: “We are actively recruiting blind people to participate in our research and we are particularly keen to involve people who have been blind since birth, yet people who lost vision later in life would be welcome to contact us too.”

Provided by Queen Mary, University of London

Source: medicalxpress.com