Posts tagged neurons
Articles and news from the latest research reports.
Most songbirds learn their songs from an adult model, mostly from the father. However, there are relatively large differences in the accuracy how these songs are copied. Researchers from the Max Planck Institute for Ornithology in Seewiesen now found in juvenile zebra finches a possible mechanism that is responsible for the differences in the intensity of song learning. They provided the nerve growth factor “BDNF” to the song control system in the brain. With this treatment the learning ability in juvenile males could be enhanced in such a way that they were able to copy the songs of the father as good as it had been observed in the best learners in a zebra finch nest.
The improvement of cognitive abilities plays an important role in the therapy of neurological and psychiatric diseases. In this context research focusses more and more on the protein BDNF (Brain Derived Neurotrophic Factor). BDNF is mainly responsible for the preservation, growth and differentiation of nerve cells. Moreover, from experiments in mice it is known that BDNF enhances the ability to solve complex cognitive tasks.
In a learning experiment with zebra finches, researchers from the Max Planck Institute for Ornithology in Seewiesen in collaboration with scientists from the Free University of Amsterdam could now show for the first time in songbirds that BDNF acts as cognitive enhancer. They investigated zebra finch brother pairs that grew up with their genetic parents. In this setup juvenile birds will readily learn the songs from their fathers. However there are differences in the intensity of song learning among siblings of the same age. The worst learners have only a similarity of 20% with their fathers’ songs, whereas the best learners copy almost the entire songs of their fathers.
By now knowing the normal distribution of the learned songs within a zebra finch nest, as a next step the researchers were able to investigate the impact of BDNF on song learning. In one of the two brothers they enhanced the expression of BDNF in the song control system in the brain while the other brother did not get such a treatment. By analysing the songs the researchers found that those sons that received more BDNF had a higher similarity with the song of their fathers compared to normally reared juveniles. Remarkably, the learning efficiency in the BDNF-treated birds was as high as it has been previously observed in the best learners within the nest. This was due to an earlier onset of syllable copying in BDNF-treated birds and these birds also copied more and sang fewer improvised syllables. Therefore it is likely that the presence of BDNF in the song control system could correct possible inaccuracies in the song learning process, state the scientists around Manfred Gahr, who is the senior author of the study.
Study points to possible treatment for brain disorders
Clemson University scientists are working to determine how neurons are generated, which is vital to providing treatment for neurological disorders like Tuberous Sclerosis Complex (TSC).
TSC is a rare genetic disease that causes the growth of tumors in the brain and other vital organs and may indicate such disorders as autism, epilepsy and cognitive impairment that may arise from the abnormal generation of neurons.
“Current medicine is directed at inhibiting the mammalian target of rapamycin (mTOR), a common feature within these tumors that have abnormally high activity,” said David M. Feliciano, assistant professor of biological sciences. “However, current treatments have severe side effects, likely due to mTOR’s many functions and playing an important role in cell survival, growth and migration.”
Feliciano and colleagues published their findings in journal Cell Reports.
“Neural stem cells generate the primary communicating cells of the brain called neurons through the process of neurogenesis, yet how this is orchestrated is unknown,” said Feliciano.
The stem cells lie at the core of brain development and repair, and alterations in the cells’ self-renewal and differentiation can have major consequences for brain function at any stage of life, according to researchers.
To better understand the process of neurogenesis, the researchers used a genetic approach known as neonatal electroporation to deliver pieces of DNA into neural stem cells in young mice, which allowed them to express and control specific components of the mTOR pathway.
The researchers found that when they increase activity of the mTOR pathway, neural stem cells make neurons at the expense of making more stem cells. They also found that this phenomenon is linked to a specific mTOR target known as 4E-BP2, which regulates the production of proteins.
Ultimately, this study points to a possible new treatment, 4E-BP2, for neurodevelopmental disorders like TSC and may have fewer side effects.
Future experiments are aimed at identifying which proteins are synthesized due to this pathway in neurological disorders.
Rats! Humans and rodents face their errors
What happens when the brain recognizes an error? A new study shows that the brains of humans and rats adapt in a similar way to errors by using low-frequency brainwaves in the medial frontal cortex to synchronize neurons in the motor cortex. The finding could be important in studies of “adaptive control” like obsessive compulsive disorder, ADHD, and Parkinson’s.
People and rats may think alike when they’ve made a mistake and are trying to adjust their thinking.
That’s the conclusion of a study published online Oct. 20 in Nature Neuroscience that tracked specific similarities in how human and rodent subjects adapted to errors as they performed a simple time estimation task. When members of either species made a mistake in the trials, electrode recordings showed that they employed low-frequency brainwaves in the medial frontal cortex (MFC) of the brain to synchronize neurons in their motor cortex. That action correlated with subsequent performance improvements on the task.
“These findings suggest that neuronal activity in the MFC encodes information that is involved in monitoring performance and could influence the control of response adjustments by the motor cortex,” wrote the authors, who performed the research at Brown University and Yale University.
The importance of the findings extends beyond a basic understanding of cognition, because they suggest that rat models could be a useful analog for humans in studies of how such “adaptive control” neural mechanics are compromised in psychiatric diseases.
“With this rat model of adaptive control, we are now able to examine whether novel drugs or other treatment procedures boost the integrity of this system,” said James Cavanagh, co-lead author of the paper who was at Brown when the research was done and has since become assistant professor of psychology at the University of New Mexico. “This may have clear translational potential for treating psychiatric diseases such as obsessive compulsive disorder, depression, attention deficit hyperactivity disorder, Parkinson’s disease and schizophrenia.”
To conduct the study, the researchers measured external brainwaves of human and rodent subjects after both erroneous and accurate performance on the time estimation task. They also measured the activity of individual neurons in the MFC and motor cortex of the rats in both post-error and post-correct circumstances.
The scientists also gave the rats a drug that blocked activity of the MFC. What they saw in those rats compared to rats who didn’t get the drug, was that the low-frequency waves did not occur in the motor cortex, neurons there did not fire coherently and the rats did not alter their subsequent behavior on the task.
Although the researchers were able to study the cognitive mechanisms in the rats in more detail than in humans, the direct parallels they saw in the neural mechanics of adaptive control were significant.
“Low-frequency oscillations facilitate synchronization among brain networks for representing and exerting adaptive control, including top-down regulation of behavior in the mammalian brain,” they wrote.
Neuron ‘claws’ in the brain enable flies to distinguish one scent from another
Think of the smell of an orange, a lemon, and a grapefruit. Each has strong acidic notes mixed with sweetness. And yet each fresh, bright scent is distinguishable from its relatives. These fruits smell similar because they share many chemical compounds. How, then does the brain tell them apart? How does the brain remember a complex and often overlapping chemical signature as a particular scent?
Researchers at Cold Spring Harbor Laboratory (CSHL) are using the fruit fly to discover how the brain integrates multiple signals to identify one unique smell. It’s work that has a broader implication for how flies – and ultimately, people – learn. In work published today in Nature Neuroscience, a team led by Associate Professor Glenn Turner describes how a group of neurons in the fruit fly brain recognize multiple individual chemicals in combination in order to define, or remember, a single scent.
The olfactory system of a fruit fly begins at the equivalent of our nose, where a series of neurons sense and respond to very specific chemicals. These neurons pass their signal on to a group of cells called projection neurons. Then the signal undergoes a transformation as it is passed to a body of neurons in the fly brain called Kenyon cells.
Kenyon cells have multiple, extremely large protrusions that grasp the projection neurons with a claw-like structure. Each Kenyon cell claw is wrapped tightly around only one projection neuron, meaning that it receives a signal from just one type of input. In addition to their unique structure, Kenyon cells are also remarkable for their selectivity. Because they’re selective, they aren’t often activated. Yet little is known about what in fact makes them decide to fire a signal.
Turner and colleague Eyal Gruntman, who is lead author on their new paper, used cutting-edge microscopy to explore the chemical response profile for multiple claws on one Kenyon cell. They found that each claw, even on a single Kenyon cell, responded to different odor molecules. Additional experiments using light to stimulate individual neurons (a technique called optogenetics) revealed that single Kenyon cells were only activated when several of their claws were simultaneously stimulated, explaining why they so rarely fire. Taken together, this work explains how individual Kenyon cells can integrate multiple signals in the brain to “remember” the particular chemical mixture as a single, distinct odor.
Turner will next try to determine “what controls which claws are connected, and how strong those connections are.” This will provide insight into how the brain learns to assign a specific mix of chemicals as defining a particular scent. But beyond simple odor detection, the research has more general implications for learning. For Turner, the question driving his work forward is: what in the brain changes when you learn something?
Researchers make exciting discoveries in non-excitable cells
It has been 60 years since scientists discovered that sodium channels create the electrical impulses crucial to the function of nerve, brain, and heart cells — all of which are termed “excitable.” Now researchers at Yale and elsewhere are discovering that sodium channels also play key roles in so-called non-excitable cells.
In the Oct. 16 issue of the journal Neuron, Yale neuroscientists Stephen Waxman and Joel Black review nearly a quarter-century of research that shows sodium channels in cells that do not transmit electrical impulses may nonetheless play a role in immune system function, migration of cells, neurodegenerative disease, and cancer.
“This insight has opened up new avenues of research in a variety of pathologies,” Waxman said.
For instance, Waxman’s lab has begun to study the functional role of voltage-gated sodium channels in non-excitable glial cells within the spinal cord and brain. They are currently investigating whether sodium channels in these non-excitable cells may participate in the formation of glial scars, thereby inhibiting regeneration of nerve cells after traumatic injury to the spinal cord or brain.
Scientists expand the genetic code of mammals to control protein activity in neurons with light
With the flick of a light switch, researchers at the Salk Institute for Biological Studies can change the shape of a protein in the brain of a mouse, turning on the protein at the precise moment they want. This allows the scientists to observe the exact effect of the protein’s activation. The new method, described in the Oct. 16, 2013, issue of the journal Neuron, relies on specially engineered amino acids—the molecules that make up proteins—and light from an LED. Now that it has been shown to work, the technique can be adapted to give researchers control of a wide variety of other proteins in the brain to study their functions.
"What we are now able to do is not only control neuronal activity, but control a specific protein within a neuron," says senior study author Lei Wang, an associate professor in Salk’s Jack H. Skirball Center for Chemical Biology and Proteomics and holder of the Frederick B. Rentschler Developmental Chair.
If a scientist wants to know what set of neurons in the brain is responsible for a particular action or behavior, being able to turn the neurons on and off at will gives the researcher a targeted way to test the neurons’ effects. Likewise, if they want to know the role of a certain protein inside the cells, the ability to activate or inactivate the protein of interest is key to studying its biology.
Over the past decade, researchers have developed a handful of ways of activating or inactivating neurons using light, as part of the burgeoning field of so-called optogenetics. In optogenetic experiments, mice are genetically engineered to have a light-sensitive channel from algae integrated into their neurons. When exposed to light, the channel opens or closes, changing the flow of molecules into the neuron and altering its ability to pass an electrochemical message through the brain. Using such optogenetic approaches, scientists can pick and choose which neurons in the brain they want turned on or off at any given time and observe the resulting change in the engineered mice.
"There’s no question that this is a great way to control neuronal activity, by borrowing light-responsive channels or pumps from other organisms and putting them in neurons," says Wang. "But rather than put a stranger into neurons, we wanted to control the activity of proteins native to neurons."
To make proteins respond to light, Wang’s team harnessed a photo-responsive amino acid, called Cmn, which has a large chemical structure. When a pulse of light shines on the molecule, Cmn’s bulky side chain breaks off, leaving cysteine, a smaller amino acid. Wang’s group realized that if a single Cmn was integrated into the right place in the structure of a protein, the drastic change in the amino acid’s size could activate or inactivate the entire protein.
To test their idea, Wang and his colleagues engineered new versions of a potassium channel in neurons, adding Cmn to their sequence.
"Basically the idea was that when you put this amino acid in the pore of the channel, the bulky side chain entirely blocks the passage of ions through the channel," explains Ji-Yong Kang, a graduate student who works in Wang’s group, and first author of the new paper. "Then, when the bond in the amino acid breaks in response to light, the channel is opened up."
The method worked in isolated cells: after trial and error, the scientists found the ideal spot in the channel to put Cmn, so that the channel was initially blocked, but opened when light shone on it. They were able to measure the change to the channel’s properties by recording the electrical current that flowed through the cells before and after exposure to light.
But to apply the technique to living mice, Wang and his colleagues needed to change the animals’ genetic code—the built-in instructions that cells use to produce proteins based on gene sequences. The normal genetic code doesn’t contain information on Cmn, so simply injecting Cmn amino acids into mice wouldn’t lead to the molecules being integrated into proteins. In the past, the Wang group and others have expanded the genetic codes of isolated cells of simple organisms like bacteria, or yeast, inserting instructions for a new amino acid. But the approach had never been successful in mammals. Through a combination of techniques and new tricks, however, Wang’s team was able to provide embryonic mice with the instructions for the new amino acid, Cmn. With the help from Salk Professor Dennis O’Leary and his research associate Daichi Kawaguchi, they then integrated the new Cmn-containing channel into the brains of the developing mice, and showed that by shining light on the brain tissue they could force the channel open, altering patterns of neuron activity. It was not only a first for expanding the genetic code of mammals, but also for protein control.
At the surface, the new approach has the same result as optogenetic approaches to studying the brain—neurons are silenced at a precise time in response to light. But Wang’s method can now be used to study a whole cadre of different proteins in neurons. Aside from being used to open and close channels or pores that let ions flow in and out of brain cells, Cmn could be used to optically regulate protein modifications and protein-protein interactions.
"We can pinpoint exactly which protein, or even which part of a protein, is crucial for the functioning of targeted neurons," says Wang. "If you want to study something like the mechanism of memory formation, it’s not always just a matter of finding what neurons are responsible, but what molecules within those neurons are critical."
Earlier this year, President Obama announced the multi-billion dollar Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, a ten-year project to map the activity of the human brain. Creating new ways to study the molecules in the brain, such as using light-responsive amino acids to study neuronal proteins, will be key to moving forward on this initiative and similar efforts to understand the brain, says Wang. His lab is now working to develop ways to not only activate proteins, but inactive them using light-sensitive amino acids, and applying the technique to proteins other than Kir2.1.
Bird study finds key info about human speech-language development
A study led by Xiaoching Li, PhD, at the LSU Health Sciences Center New Orleans Neuroscience Center of Excellence, has shown for the first time how two tiny molecules regulate a gene implicated in speech and language impairments as well as autism disorders, and that social context of vocal behavior governs their function. The findings are published in the October 16, 2013 issue of The Journal of Neuroscience.
Speech and language impairments affect the lives of millions of people, but the underlying neural mechanisms are largely unknown and difficult to study in humans. Zebra finches learn to sing and use songs for social communications. Because the vocal learning process in birds has many similarities with speech and language development in humans, the zebra finch provides a useful model to study the neural mechanisms underlying speech and language in humans.
Mutations in the FOXP2 gene have been linked to speech and language deficits and in autism disorders. A current theory is that a precise amount of FOXP2 is required for the proper development of the neural circuits processing speech and language, so it is important to understand how the FOXP2 gene is regulated. In this study, the research team identified two microRNAs, or miRNAs, – miR-9 and miR-140-5p – that regulate the levels of FOXP2. (MicroRNAs are a new class of small RNA molecules that play an important regulatory role in cell biology. They prevent the production of a particular protein by binding to and destroying the messenger RNA that would have produced the protein.) The researchers showed that in the zebra finch brain, these miRNAs are expressed in a basal ganglia nucleus that is required for vocal learning, and their function is regulated during vocal learning. More intriguingly, the expression of these two miRNAs is also regulated by the social context of song behavior – in males singing undirected songs.
"Because the FOXP2 gene and these two miRNAs are evolutionarily conserved, the insights we obtained from studying birds are highly relevant to speech and language in humans and related neural developmental disorders such as autism," notes Xiaoching Li, PhD,
LSUHSC Assistant Professor of Cell Biology and Anatomy as well as Neuroscience. “Understanding how miRNAs regulate FOXP2 may open many possibilities to influence speech and language development through genetic variations in miRNA genes, as well as behavioral and environmental factors.”
‘Individualized’ Therapy for the Brain Targets Specific Gene Mutations Causing Dementia and ALS
Johns Hopkins scientists have developed new drugs that — at least in a laboratory dish — appear to halt the brain-destroying impact of a genetic mutation at work in some forms of two incurable diseases, amyotrophic lateral sclerosis (ALS) and dementia.
They made the finding by using neurons they created from stem cells known as induced pluripotent stem cells (iPS cells), which are derived from the skin of people with ALS who have a gene mutation that interferes with the process of making proteins needed for normal neuron function.
“Efforts to treat neurodegenerative diseases have the highest failure rate for all clinical trials,” says Jeffrey D. Rothstein, M.D., Ph.D., a professor of neurology and neuroscience at the Johns Hopkins University School of Medicine and leader of the research described online in the journal Neuron. “But with this iPS technology, we think we can target an exact subset of patients with a specific mutation and succeed. It’s individualized brain therapy, just the sort of thing that has been done in cancer, but not yet in neurology.”
Scientists in 2011 discovered that more than 40 percent of patients with an inherited form of ALS and at least 10 percent of patients with the non-inherited sporadic form have a mutation in the C9ORF72 gene. The mutation also occurs very often in people with frontotemporal dementia, the second-most-common form of dementia after Alzheimer’s disease. The same research appeared to explain why some people develop both ALS and the dementia simultaneously and that, in some families, one sibling might develop ALS while another might develop dementia.
In the C9ORF72 gene of a normal person, there are up to 30 repeats of a series of six DNA letters (GGGGCC); but in people with the genetic glitch, the string can be repeated thousands of times. Rothstein, who is also director of the Johns Hopkins Brain Science Institute and the Robert Packard Center for ALS Research, used his large bank of iPS cell lines from ALS patients to identify several with the C9ORF72 mutation, then experimented with them to figure out the mechanism by which the “repeats” were causing the brain cell death characteristic of ALS.
In a series of experiments, Rothstein says, they discovered that in iPS neurons with the mutation, the process of using the DNA blueprint to make RNA and then produce protein is disrupted. Normally, RNA-binding proteins facilitate the production of RNA. Instead, in the iPS neurons with the C9ORF72 mutation, the RNA made from the repeating GGGGCC strings was bunching up, gumming up the works by acting like flypaper and grabbing hold of the extremely important RNA binding proteins, including one known as ADARB2, needed for the proper production of many other cellular RNAs. Overall, the C9ORF72 mutation made the cell produce abnormal amounts of many other normal RNAs and made the cells very sensitive to stress.
To counter this effect, the researchers developed a number of chemical compounds targeting the problem. This compound behaved like a coating that matches up to the GGGGCC repeats like velcro, keeping the flypaper-like repeats from attracting the bait, allowing the RNA-binding protein to properly do its job.
Rothstein says Isis Pharmaceuticals helped develop many of the studied compounds and, by working closely with the Johns Hopkins teams, could begin testing it in human ALS patients with the C9ORF72 mutation in the next several years. In collaboration with the National Institutes of Health, plans are already underway to begin to identify a group of patients with the C9ORF72 mutation for future research.
Rita Sattler, Ph.D., an assistant professor of neurology at Johns Hopkins and the co-investigator of the study, says without iPS technology, the team would have had a difficult time studying the C9ORF72 mutation. “Typically, researchers engineer rodents with mutations that mimic the human glitches they are trying to research and then study them,” she says. “But the nature of the multiple repeats made that nearly impossible.” The iPS cells did the job just as well or even better than an animal model, Sattler says, in part because the experiments could be done using human cells.
“An iPS cell line can be used effectively and rapidly to understand disease mechanisms and as a tool for therapy development,” Rothstein adds. “Now we need to see if our findings translate into a valuable treatment for humans.”
The researchers also analyzed brain tissue from people with the C9ORF72 mutation who died of ALS. They saw evidence of this bunching up and found that the many genes that were altered as a consequence of this mutation in the iPS cells were also abnormal in the brain tissue, thereby showing that iPS cells can be a faithful tool to study the human disease and discover effective therapies.
In the future, the scientists will look at cerebral spinal fluid from ALS patients with the C9ORF72 mutation, searching for proteins that were found both in the fluid and the iPS cells. These may pave the way to develop markers that can be studied by clinicians to see if the treatment is working once the drug therapy is moved to clinical trials.
ALS, sometimes known as Lou Gehrig’s disease, named for the Yankee baseball great who died from it, destroys nerve cells in the brain and spinal cord that control voluntary muscle movement. The nerve cells waste away or die, and can no longer send messages to muscles, eventually leading to muscle weakening, twitching and an inability to move the arms, legs and body. Onset is typically around age 50 and death often occurs within three to five years of diagnosis. Some 10 percent of cases are hereditary. There is no cure for ALS and there is only one FDA-approved drug treatment, which has just a small effect in slowing disease progression and increasing survival, Rothstein notes.
(Source: hopkinsmedicine.org)
Scientists unravel mechanisms in chronic itching
Anyone who has suffered through sleepless nights due to uncontrollable itching knows that not all itching is the same. New research at Washington University School of Medicine in St. Louis explains why.
Working in mice, the scientists have shown that chronic itching, which can occur in many medical conditions, from eczema and psoriasis to kidney failure and liver disease, is different from the fleeting urge to scratch a mosquito bite.
That’s because chronic itching appears to incorporate more than just the nerve cells, or neurons, that normally transmit itch signals. The researchers found that in chronic itching, neurons that send itch signals also co-opt pain neurons to intensify the itch sensation.
The new discovery may lead to more effective treatments for chronic itching that target activity in neurons involved in both pain and itch. The research is reported online Oct. 15 in The Journal of Clinical Investigation and will appear in the November print issue.
“In normal itching, there’s a fixed pathway that transmits the itch signal,” said senior investigator Zhou-Feng Chen, PhD, who directs Washington University’s Center for the Study of Itch. “But with chronic itching, many neurons can be turned into itch neurons, including those that typically transmit pain signals. That helps explain why chronic itching can be so excruciating.”
Chen, a professor of anesthesiology, and his colleagues generated mice in which a protein called BRAF always is active and continually sends signals inside itch neurons. The BRAF gene and the protein it makes are involved in the body’s pain response, but scientists didn’t know whether the gene also played a role in itch.
“We thought the animals might be prone to feeling pain rather than itching,” Chen explained. “To our great surprise, the mice scratched spontaneously. At first, we didn’t know why they were scratching, but it turns out we developed a mouse model of chronic itch.”
Further studies discovered that the BRAF protein could turn on many itch genes, and they showed similar changes of gene expression in mice with chronic itch induced by dry skin and in mice with allergic contact dermatitis, two of the skin conditions that frequently cause people to scratch incessantly.
The findings suggest that targeting proteins in the BRAF pathway may open new avenues for treating chronic itch, a condition in which few therapies are effective. One possibility includes using drugs that are prescribed to treat pain.
“Certain drugs are used to inhibit some of the same targets in patients with chronic pain, and those medications also may quiet down itch,” Chen said.
In earlier studies, Chen identified gastrin-releasing peptide (GRP), a substance that carries itch signals to a gene called GRPR (gastrin-releasing peptide receptor) in the spinal cord. In the new study, GRP and GRPR activity was doubled in the genetically altered mice, which could account for some of the increase in the intensity of itching. But other genes that normally are activated by pain also were turned on in the itch pathway, further intensifying the itch sensation.
Surprisingly, however, the mice had a normal response to pain, indicating that the pain and itch pathways are very different.
Unlike scratching a mosquito bite, which usually is only a temporary sensation, chronic itch can persist much longer, according to Chen, also a professor of psychiatry and of developmental biology. His team found that the mice in this study not only scratched spontaneously but also had more severe responses when exposed to substances that normally would induce acute itching.
“In people, chronic itching can last for weeks, months or even years,” Chen said. “These mice are helping us to understand the pathways that can be involved in transmitting itch signals and the many contributors to chronic itching. There are many pathways leading from BRAF, and all of these could be potential targets for anti-itch therapies.”
(Source: news.wustl.edu)
Genetic identification of a neural circuit that suppresses appetite
Scientists at the University of Washington have used genetic engineering to identify a population of neurons that tell the brain to shut off appetite. Their study, “Genetic identification of a neural circuit that suppresses appetite,” was published Oct. 13 in Nature.
To identify these neurons, or cells that process and transmit information in the brain, researchers first considered what makes an animal lose its appetite. There are a number of natural reasons, including infection, nausea, pain or simply having eaten too much already.
Nerves within the gut that are distressed or insulted send information to the brain through the vagus nerve. Appetite is suppressed when these messages activate specific neurons – ones that contain CGRP, (calcitonin gene-related peptide) in a region of the brain called the parabrachial nucleus.
In mouse trials, researchers used genetic techniques and viruses to introduce light-activatable proteins into CGRP neurons. Activation of these proteins excites the cells to transmit chemical signals to other regions of the brain. When they activated the CGRP neurons with a laser, the hungry mice immediately lost their appetite and walked away from their liquid diet (Ensure); when the laser was turned off, the mice resumed drinking the liquid diet.
"These results demonstrate that activation of the CGRP-expressing neurons regulates appetite. This is a nice example of how the brain responds to unfavorable conditions in the body, such as nausea caused by food poisoning" said Richard Palmiter, UW professor of biochemistry and investigator of the Howard Hughes Medical Institute.
Using a similar approach, neurons in other brain regions have been identified that can stimulate the appetite of mice that are not hungry. Researchers hope to identify the complete neural circuit (wiring diagram) in the brain that regulates feeding behavior. By identifying these neural circuits, scientists may be able to design therapies that promote or decrease appetite.
(Source: eurekalert.org)