Posts tagged plasticity

Posts tagged plasticity
Researchers at the University of Glasgow are hoping to help victims of stroke to overcome physical disabilities by helping their brains to ‘rewire’ themselves.
Doctors and scientists from the Institute of Cardiovascular and Medical Sciences will undertake the world’s first in-human trial of vagus nerve stimulation in stroke patients. Stroke can result in the loss of brain tissue and negatively affect various bodily functions from speech to movement, depending on the location of the stroke.
The study, which will be carried out at the Western Infirmary in Glasgow, will recruit 20 patients who suffered a stroke around six months ago and who have been left with poor arm function as a result.
Each participant will receive three one-hour sessions of intensive physiotherapy each week for six weeks to help improve their arm function.
Half of the group will also receive an implanted Vivistim device, a vagus nerve stimulator, which connects to the vagus nerve in the neck. When they are receiving physiotherapy to help improve their arm, the device will stimulate the nerve.
It is hoped that this will stimulate release of the brain’s own chemicals, called neurotransmitters, that will help the brain form new neural connections which might improve participants ability to use their arm.
Lead researcher Dr Jesse Dawson, a Stroke Specialist and Clinical Senior Lecturer in Medicine, said: “When the brain is damaged by stroke, important neural connections that control different parts of the body can be damaged which impairs function.
“Evidence from animal studies suggests that vagus nerve stimulation could cause the release of neurotransmitters which help facilitate neural plasticity and help people re-learn how to use their arms after stroke; particularly if stimulation is paired with specific tasks. A slightly different type of vagus nerve stimulation is already successfully used to manage conditions such as depression and epilepsy.
“This study is designed to provide evidence to support whether this is the case after stroke but our primary aim is to assess feasibility of vagus nerve stimulation after stroke.
“It remains to be seen how much we can improve function, but if we can help people perform even small actions again, like being able to hold a cup of tea, it would greatly improve their quality of life.”
(Source: gla.ac.uk)
Researcher Finds Gender Differences In Seasonal Auditory Changes
Auditory systems differ between sexes in sparrows depending on the season, a Georgia State University neuroscientist has found. The work adds to our knowledge of how the parts of the nervous system, including that of humans, are able to change.
Megan Gall, a post-doctoral researcher with Georgia State’s Neuroscience Institute, tested the peripheral auditory systems of male and female house sparrows, comparing the hearing of each gender during non-breeding seasons and breeding seasons.
Gall measured frequency selectivity – the ability to tell sounds that are close in frequency apart, and temporal resolution, the ability to tell sounds apart that are very close together in time.
“We found that males have the same frequency selectivity and temporal resolution across breeding seasons,” Gall said. “In the fall, males and females aren’t different. But in the breeding season, females had better frequency selectivity, but this came at the expense of worse temporal resolution.”
The study was published in the Proceedings of The Royal Society B, a British scientific journal.
The difference shows “plasticity,” the ability to change, she said. Plasticity is an important concept in neuroscience, as scientists have increasingly been able to show that neurological systems have the ability to change.
Gall said the work shows, for the first time, that there’s seasonal plasticity in these properties in the periphery of the auditory system, the ear and the auditory nerve, not just inside the parts of the brain that control auditory function.
Similar changes happen in humans, she said. Women show different auditory sensitivities during the course of a menstrual cycle. “I always like to say that if your husband says he can’t hear you, it may be that he can’t. His auditory system is different than yours,” Gall said.
The changes might have evolved over time for different reasons, she said, with one reason being that it is harder for the body to maintain a certain kind of tissues involved in hearing.
Research may prompt new investigations into white matter’s role in psychiatric disorders as well as connections between mood and myelin diseases, like MS
Animals that are socially isolated for prolonged periods make less myelin in the region of the brain responsible for complex emotional and cognitive behavior, researchers at the University at Buffalo and Mt. Sinai School of Medicine report in Nature Neuroscience online.
The research sheds new light on brain plasticity, the brain’s ability to adapt to environmental changes. It reveals that neurons aren’t the only brain structures that undergo changes in response to an individual’s environment and experience, according to one of the paper’s lead authors, Karen Dietz, PhD, research scientist in the Department of Pharmacology and Toxicology in the UB School of Medicine and Biomedical Sciences.
Dietz did the work while a postdoctoral researcher at Mt. Sinai School of Medicine; Jia Liu, PhD, a Mt. Sinai postdoctoral researcher, is the other lead author.
The paper notes that changes in the brain’s white matter, or myelin, have been seen before in psychiatric disorders, and demyelinating disorders have also had an association with depression. Recently, myelin changes were also seen in very young animals or adolescents responding to environmental changes.
"This research reveals for the first time a role for myelin in adult psychiatric disorders," Dietz says. "It demonstrates that plasticity in the brain is not restricted to neurons, but actively occurs in glial cells, such as the oligodendrocytes, which produce myelin."
(Source: eurekalert.org)
Brain connectivity predicts reading skills
The growth pattern of long-range connections in the brain predicts how a child’s reading skills will develop, according to research published today in Proceedings of the National Academy of Sciences
Literacy requires the integration of activity in brain areas involved in vision, hearing and language. These areas are distributed throughout the brain, so efficient communication between them is essential for proficient reading.
Jason Yeatman, a neuroscientist at Stanford University in California, and his colleagues studied how the development of reading ability relates to growth in the brain’s white-matter tracts, the bundles of nerve fibres that connect distant regions of the brain.
They tested how the reading skills of 55 children aged between 7 and 12 years old developed over a three-year period. There were big differences in reading ability between the children, and these differences persisted — the children who were weak readers relative to their peers at the beginning of the study were still weak three years later.
The researchers also scanned the brains of 39 of the children at least three times during the same period, to visualize the growth of two major white-matter tracts: the arcuate fasciculus, which conects the brain’s language centres, and the inferior longitudinal fasciculus, which links the language centres with the parts of the brain that process visual information.
Differences in the growth of both tracts could predict the variations in reading ability. Strong readers started off with a weak signal in both tracts on the left side of the brain, which got stronger over the three years. Weaker readers exhibited the opposite pattern.
Research identifies the mechanism that protects our brains from turning stress and trauma into post-traumatic stress disorder
Researchers from the University of Exeter Medical School have for the first time identified the mechanism that protects us from developing uncontrollable fear.
Our brains have the extraordinary capacity to adapt to changing environments – experts call this ‘plasticity’. Plasticity protects us from developing mental disorders as the result of stress and trauma.
Researchers found that stressful events re-programme certain receptors in the emotional centre of the brain (the amygdala), which the receptors then determine how the brain reacts to the next traumatic event.
These receptors (called protease-activated receptor 1 or PAR1) act in the same way as a command centre, telling neurons whether they should stop or accelerate their activity.
Before a traumatic event, PAR1s usually tell amygdala neurons to remain active and produce vivid emotions. However, after trauma they command these neurons to stop activating and stop producing emotions – so protecting us from developing uncontrollable fear.
This helps us to keep our fear under control, and not to develop exaggerated responses to mild or irrelevant fear triggers – for example, someone who may have witnessed a road traffic accident who develops a fear of cars or someone who may have had a dog jump up on them as a child and who now panics when they see another dog.
The research team used mice in which the PAR1 receptors were genetically de-activated and found that the animals developed a pathological fear in response to even mild, aversive stimuli.
The study was led by Professor Robert Pawlak of University of Exeter Medical School. He said: “The discovery that the same receptor can either awaken neurons or ‘switch them off’ depending on previous trauma and stress experience, adds an entirely new dimension to our knowledge of how the brain operates and emotions are formed.”
Professor Pawlak added: “We are now planning to extend our study to investigate if the above mechanisms, or genetic defects of the PAR1 receptor, are responsible for the development of anxiety disorders and depression in human patients. There is more work to be done, but the potential for the development of future therapies based on our findings is both exciting and intriguing.”
The article describing the above findings has recently been published in one of the most prestigious psychiatry journals, Molecular Psychiatry.
(Source: eurekalert.org)
Strokes often cause loss or impairment of vital brain functions – such as speech, movement, vision or attention. Restoration of these functions is often possible, but difficult. One of the factors impeding brain plasticity is inflammation. A study on rats, carried out at the Nencki Institute in Warsaw, suggests that effectiveness of neurorehabilitation after a stroke can be improved by anti-inflammatory drugs.
Post-stroke inflammation slows down recovery and impairs brain plasticity, reveal the results from the lab of Professor Małgorzata Kossut at the Nencki Institute in Warsaw. The popular anti-inflammatory drug ibuprofen restores the ability of brain cortex to reorganize – a process necessary for recovery of stroke-damaged functions. “Our research was conducted on rats, but we have good reasons to suppose that in future our results will help improve effectiveness of rehabilitation of stroke patients”, says Prof. Kossut.
The Nencki Institute team stresses that so far there are no proofs that the treatment will be effective in humans and that they did not investigate if the ibuprofen therapy prevents strokes, but concentrated on post-stroke recovery.
The most frequent cause of stroke is blocking of brain arteries. Without supply of oxygen, neurons die quckly. In the region of stroke-induced damage pathological changes cause decrease of brain tissue metabolism, impairment of neurotransmission and edema.
Brain control over physiological and voluntary functions may be lost, depending on the localization of the infarct. Impairments of movement, vision, speech and attention are frequent. In most cases these functions return either partially or completely. Sometimes they return spontaneously, more often after neurorehabilitation.
“In both instances recovery is based on neuroplasticity, the ability of the brain to reorganize, that is to change the properties of neurons and to alter the connections between them”, says Dr. Monika Liguz-Lęcznar (Nencki Institute).
After a stroke, neuroplasticity is impaired. Scientists from the Nencki Institute suppose that this may be due to inflammation developing at the site of the stroke. The proof that decreasing inflammation helps neurorehabilitation came from experiments done on rats with experimentally induced stroke. The stroke was localized in a special region of the brain cortex, receiving information from whiskers.
The whiskers are important sensory organs of rodents, allowing the animals to orient themselves in their environment in darkness. Every whisker activates a small, precisely delineated chunk of brain cortex.
In healthy rats neuroplastic changes can be induced by cutting off some of the whiskers, that is by eliminating part of the sensory input to the brain. The brain reacts to that by letting the remaining whiskers take over more cortical space, expand their cortical representation, at the expense of the cut off ones.
“This plastic change does not occur when the site of stroke-induced damage is near the region of cortex ‘belonging’ to the whiskers. We showed that application of ibuprofen decreases inflammation and restores neuroplasticity – the brain cortex reorganizes like in healthy animals”, says Prof. Kossut.
(Source: press.nencki.gov.pl)
Most people equate “gray matter” with the brain and its higher functions, such as sensation and perception, but this is only one part of the anatomical puzzle inside our heads. Another cerebral component is the white matter, which makes up about half the brain by volume and serves as the communications network.
The gray matter, with its densely packed nerve cell bodies, does the thinking, the computing, the decision-making. But projecting from these cell bodies are the axons—the network cables. They constitute the white matter. Its color derives from myelin—a fat that wraps around the axons, acting like insulation.
Alex Schelgel, first author on a paper in the August 2012 Journal of Cognitive Neuroscience, has been using the white matter as a landscape on which to study brain function. An important result of the research is showing that you can indeed “teach old dogs new tricks.” The brain you have as an adult is not necessarily the brain you are always going to have. It can still change, even for the better.
"This work is contributing to a new understanding that the brain stays this plastic organ throughout your life, capable of change," Schlegel says. "Knowing what actually happens in the organization of the brain when you are learning has implications for the development of new models of learning as well as potential interventions in cases of stroke and brain damage."
Schlegel is a graduate student working under Peter Tse, an associate professor of psychological and brain sciences and a coauthor on the paper. “This study was Peter’s idea,” Schlegel says. “He wanted to know if we could see white matter change as a result of a long-term learning process. Chinese seemed to him like the most intensive learning experience he could think of.”
Twenty-seven Dartmouth students were enrolled in a nine-month Chinese language course between 2007 and 2009, enabling Schlegel to study their white matter in action. While many neuroscientists use magnetic resonance imaging (MRI) in brain studies, Schlegel turned to a new MRI technology, called diffusion tensor imaging (DTI). He used DTI to measure the diffusion of water in axons, tracking the communication pathways in the brain. Restrictions in this diffusion can indicate that more myelin has wrapped around an axon.
"An increase in myelination tells us that axons are being used more, transmitting messages between processing areas," Schlegel says. "It means there is an active process under way."
Their data suggest that white matter myelination is precisely what was seen among the language students. There is a structural change that goes along with this learning process. While some studies have shown that changes in white matter occurred with learning, these observations were made in simple skill learning and strictly on a “before and after” basis.
"This was the first study looking at a really complex, long-term learning process over time, actually looking at changes in individuals as they learn a task," says Schlegel. "You have a much stronger causal argument when you can do that."
The work demonstrates that significant changes are occurring in adults who are learning. The structure of their brains undergoes change.
"This flies in the face of all these traditional views that all structural development happens in infancy, early in childhood," Schlegel says. "Now that we actually do have tools to watch a brain change, we are discovering that in many cases the brain can be just as malleable as an adult as it is when you are a child or an adolescent."
(Source: eurekalert.org)

Sleep Oscillations in the Thalamocortical System Induce Long-Term Neuronal Plasticity
Long-term plasticity contributes to memory formation and sleep plays a critical role in memory consolidation. However, it is unclear whether sleep slow oscillation by itself induces long-term plasticity that contributes to memory retention. Using in vivo prethalamic electrical stimulation at 1 Hz, which itself does not induce immediate potentiation of evoked responses, we investigated how the cortical evoked response was modulated by different states of vigilance. We found that somatosensory evoked potentials during wake were enhanced after a slow-wave sleep episode (with or without stimulation during sleep) as compared to a previous wake episode. In vitro, we determined that this enhancement has a postsynaptic mechanism that is calcium dependent, requires hyperpolarization periods (slow waves), and requires a coactivation of both AMPA and NMDA receptors. Our results suggest that long-term potentiation occurs during slow-wave sleep, supporting its contribution to memory.
Plasticity of Inhibition
Until recently, the study of plasticity of neural circuits focused almost exclusively on potentiation and depression at excitatory synapses on principal cells. Other elements in the neural circuitry, such as inhibitory synapses on principal cells and the synapses recruiting interneurons, were assumed to be relatively inflexible, as befits a role of inhibition in maintaining stable levels and accurate timing of neuronal activity. It is now evident that inhibition is highly plastic, with multiple underlying cellular mechanisms. This Review considers these recent developments, focusing mainly on functional and structural changes in GABAergic inhibition of principal cells and long-term plasticity of glutamateric recruitment of inhibitory interneurons in the mammalian forebrain. A major challenge is to identify the adaptive roles of these different forms of plasticity, taking into account the roles of inhibition in the regulation of excitability, generation of population oscillations, and precise timing of neuronal firing.
Re-opening Windows: Manipulating Critical Periods for Brain Development
The brain acquires certain skills—from visual perception to language—during critical windows, specific times in early life when the brain is actively shaped by environmental input. Scientists like Takao K. Hensch are now discovering pathways in animal models through which these windows might be re-opened in adults, thus re-awakening a brain’s youth-like plasticity. Such research has implications for brain injury repair, sensory recovery, and neurodevelopmental disorder treatment. In addition, what we know today about these critical windows of development already has enormous implications for social and educational policy.