Posts tagged neuron
Articles and news from the latest research reports.
A circuit diagram of the mouse brain
What happens in the brain when we see, hear, think and remember? To be able to answer questions like this, neuroscientists need information about how the millions of neurons in the brain are connected to each other. Scientists at the Max Planck Institute for Medical Research in Heidelberg have taken a crucial step towards obtaining a complete circuit diagram of the brain of the mouse, a key model organism for the neurosciences. The research group working with Winfried Denk has developed a method for preparing the whole mouse brain for a special microscopy process. With this, the resolution at which the brain tissue can be examined is so high that the fine extensions of almost every single neuron are visible.
How the brain forms categories
Neurobiologists at the Research Institute of Molecular Pathology (IMP) in Vienna investigated how the brain is able to group external stimuli into stable categories. They found the answer in the discrete dynamics of neuronal circuits. The journal Neuron publishes the results in its current issue.
How do we manage to recognize a friend’s face, regardless of the light conditions, the person’s hairstyle or make-up? Why do we always hear the same words, whether they are spoken by a man or woman, in a loud or soft voice? It is due to the amazing skill of our brain to turn a wealth of sensory information into a number of defined categories and objects. The ability to create constants in a changing world feels natural and effortless to a human, but it is extremely difficult to train a computer to perform the task.
At the IMP in Vienna, neurobiologist Simon Rumpel and his post-doc Brice Bathellier have been able to show that certain properties of neuronal networks in the brain are responsible for the formation of categories. In experiments with mice, the researchers produced an array of sounds and monitored the activity of nerve cell-clusters in the auditory cortex. They found that groups of 50 to 100 neurons displayed only a limited number of different activity-patterns in response to the different sounds.
The scientists then selected two basis sounds that produced different response patterns and constructed linear mixtures from them. When the mixture ratio was varied continuously, the answer was not a continuous change in the activity patters of the nerve cells, but rather an abrupt transition. Such dynamic behavior is reminiscent of the behavior of artificial attractor-networks that have been suggested by computer scientists as a solution to the categorization problem.
The findings in the activity patters of neurons were backed up by behavioral experiments with mice. The animals were trained to discriminate between two sounds. They were then exposed to a third sound and their reaction was tracked. Whether the answer to the third tone was more like the reaction to the first or the second one, was used as an indicator of the similarity of perception. By looking at the activity patters in the auditory cortex, the scientists were able to predict the reaction of the mice.
The new findings that are published in the current issue of the journal Neuron, demonstrate that discrete network states provide a substrate for category formation in brain circuits. The authors suggest that the hierarchical structure of discrete representations might be essential for elaborate cognitive functions such as language processing.
(Source: alphagalileo.org)
Fear really resides in a different area of the brain than its inhibitory mechanisms
Do you suffer from a phobia? Maybe arachnophobia? Then you know very well that even if you do not feel uneasy when imagining a huge and hairy tarantula in the therapist’s office, you still jump out of the shower screaming upon seeing a tiny spider. Why is it so hard to get rid of a phobia?
Extinguishing the fear response does not consist of erasing the memory of the fear provoking stimuli, but creating new, competitive memory traces. It has been suspected for some time that neuronal brain circuits responsible for extinguishing fear differ from circuits involved in reoccurrence of the fear response. This assumption has finally been experimentally confirmed. Novel experiments, described in PNAS, a prestigious journal of the American National Academy of Sciences, have been conducted by scientists from the Nencki Institute of Experimental Biology of the Polish Academy of Sciences and the International Institute of Molecular and Cell Biology in Warsaw. This research team was headed by Dr Ewelina Knapska, Dr Jacek Jaworski and Prof. Leszek Kaczmarek.
“Research has been carried out using a special, genetically modified strain of rats developed in the Nencki Institute. As a result we were able to observe the connections between neurons activated in the brains of animals experiencing fear”, explains Dr Ewelina Knapska, head of the Laboratory of Emotions Neurobiology in the Nencki Institute.
A glance at the brain’s circuit diagram
The human brain accomplishes its remarkable feats through the interplay of an unimaginable number of neurons that are interconnected in complex networks. A team of scientists from the Max Planck Institute for Dynamics and Self-Organization, the University of Göttingen and the Bernstein Center for Computational Neuroscience Göttingen has now developed a method for decoding neural circuit diagrams. Using measurements of total neuronal activity, they can determine the probability that two neurons are connected with each other.
Study clarifies process controlling night vision
New research reveals the key chemical process that corrects for potential visual errors in low-light conditions. Understanding this fundamental step could lead to new treatments for visual deficits, or might one day boost normal night vision to new levels.
Like the mirror of a telescope pointed toward the night sky, the eye’s rod cells capture the energy of photons - the individual particles that make up light. The interaction triggers a series of chemical signals that ultimately translate the photons into the light we see.
The key light receptor in rod cells is a protein called rhodopsin. Each rod cell has about 100 million rhodopsin receptors, and each one can detect a single photon at a time.
Scientists had thought that the strength of rhodopsin’s signal determines how well we see in dim light. But UC Davis scientists have found instead that a second step acts as a gatekeeper to correct for rhodopsin errors. The result is a more accurate reading of light under dim conditions.
A report on their research appears in the October issue of the journal Neuron in a study entitled “Calcium feedback to cGMP synthesis strongly attenuates single photon responses driven by long rhodopsin lifetimes.”
Research discovers two opposite ways our brain voluntarily forgets unwanted memories
If only there were a way to forget that humiliating faux pas at last night’s dinner party. It turns out there’s not one, but two opposite ways in which the brain allows us to voluntarily forget unwanted memories, according to a study published by Cell Press October 17 in the journal Neuron. The findings may explain how individuals can cope with undesirable experiences and could lead to the development of treatments to improve disorders of memory control.
"This study is the first demonstration of two distinct mechanisms that cause such forgetting: one by shutting down the remembering system, and the other by facilitating the remembering system to occupy awareness with a substitute memory," says lead study author Roland Benoit of the MRC Cognition and Brain Sciences Unit at the University of Cambridge.
Previous studies have shown that individuals can voluntarily block memories from awareness. Although several neuroimaging studies have examined the brain systems involved in intentional forgetting, they have not revealed the cognitive tactics that people use or the precise neural underpinnings. Two possible ways to forget unwanted memories are to suppress them or to substitute them with more desirable memories, and these tactics could engage distinct neural pathways.
(Source: medicalxpress.com)
Understanding Alzheimer’s: Study gives insights into how disease kills brain cells
Exactly how Alzheimer’s disease kills brain cells is still somewhat of a mystery, but University of Michigan researchers have uncovered a clue that supports the idea that small proteins prick holes into neurons.
The team also found that a certain size range of clumps of these proteins are particularly toxic to cells, while smaller and larger aggregates of the protein appear to be benign.
The findings, which appear in the journal PLOS ONE, add important detail to the knowledge base regarding this disease that affects 5.4 million Americans in 2012 but remains incurable and largely untreatable. The results could potentially help pharmaceutical researchers target drugs to the right disease mechanisms.
Small proteins called amyloid-beta peptides are the prime suspect for causing cell death in Alzheimer’s. They make up most of the senile plaque fibers found in the brains of autopsied patients. Researchers offer several hypotheses for how the peptides might cause the disease. They blame inflammation, oxidative stress or an imbalance of calcium ions possibly caused by holes in the cell membranes.
The U-M findings strongly support the idea that amyloid peptides damage the membrane around nerve cells and lead to uncontrolled movement of calcium ions into them. Calcium signaling is an important way that cells communicate and healthy cells regulate its flow precisely. The toxic mechanism implicated in the new study could act on its own or together with the other proposed courses and ultimately lead to a loss of brain cells in patients, the researchers say.
Calcium reveals connections between neurons
A team led by MIT neuroscientists has developed a way to monitor how brain cells coordinate with each other to control specific behaviors, such as initiating movement or detecting an odor.
The researchers’ new imaging technique, based on the detection of calcium ions in neurons, could help them map the brain circuits that perform such functions. It could also provide new insights into the origins of autism, obsessive-compulsive disorder and other psychiatric diseases, says Guoping Feng, senior author of a paper appearing in the Oct. 18 issue of the journal Neuron.
“To understand psychiatric disorders we need to study animal models, and to find out what’s happening in the brain when the animal is behaving abnormally,” says Feng, the James W. and Patricia Poitras Professor of Neuroscience and a member of the McGovern Institute for Brain Research at MIT. “This is a very powerful tool that will really help us understand animal models of these diseases and study how the brain functions normally and in a diseased state.”
Attack! Silent watchmen charge to defend the nervous system
In many pathologies of the nervous system, there is a common event - cells called microglia are activated from surveillant watchmen into fighters. Microglia are the immune cells of the nervous system, ingesting and destroying pathogens and damaged nerve cells. Until now little was known about the molecular mechanisms of microglia activation despite this being a critical process in the body. Now new research from the Montreal Neurological Institute and Hospital – The Neuro - at McGill University provides the first evidence that mechanisms regulated by the Runx1 gene control the balance between the surveillant versus activated microglia states. The finding, published in the Journal of Neuroscience, has significant implications for understanding and treating neurological conditions.
Neuroscientists find the molecular “When” and “Where” of memory formation
Neuroscientists from New York University and the University of California, Irvine have isolated the “when” and “where” of molecular activity that occurs in the formation of short-, intermediate-, and long-term memories. Their findings, which appear in the journal the Proceedings of the National Academy of Sciences, offer new insights into the molecular architecture of memory formation and, with it, a better roadmap for developing therapeutic interventions for related afflictions.
“Our findings provide a deeper understanding of how memories are created,” explained the research team leader Thomas Carew, a professor in NYU’s Center for Neural Science and dean of NYU’s Faculty of Arts and Science. “Memory formation is not simply a matter of turning molecules on and off; rather, it results from a complex temporal and spatial relationship of molecular interaction and movement.”
Neuroscientists have previously uncovered different aspects of molecular signaling relevant to the formation of memories. But less understood is the spatial relationship between molecules and when they are active during this process.
To address this question, the researchers studied the neurons in Aplysia californica, the California sea slug. Aplysia is a model organism that is quite powerful for this type of research because its neurons are 10 to 50 times larger than those of higher organisms, such as vertebrates, and it possesses a relatively small network of neurons—characteristics that readily allow for the examination of molecular signaling during memory formation. Moreover, its coding mechanism for memories is highly conserved in evolution, and thus is similar to that of mammals, making it an appropriate model for understanding how this process works in humans.
The scientists focused their study on two molecules, MAPK and PKA, which earlier research has shown to be involved in many forms of memory and synaptic plasticity—that is, changes in the brain that occur after neuronal interaction. But less understood was how and where these molecules interacted.
To explore this, the researchers subjected the sea slugs to sensitization training, which induces increased behavioral reflex responsiveness following mild tail shock, or in this study, mild activation of the nerve form the tail. They then examined the subsequent molecular activity of both MAPK and PKA. Both molecules have been shown to be involved in the formation of memory for sensitization, but the nature of their interaction is less clear.
What they found was MAPK and PKA coordinate their activity both spatially and temporally in the formation of memories. Specifically, in the formation of intermediate-term (i.e., hours) and long-term (i.e., days) memories, both MAPK and PKA activity occur, with MAPK spurring PKA action. By contrast, for short-term memories (i.e., less than 30 minutes), only PKA is active, with no involvement of MAPK.
(Source: nyu.edu)