Posts tagged neuroscience
Articles and news from the latest research reports.
E-Whiskers: Berkeley Researchers Develop Highly Sensitive Tactile Sensors for Robotics and Other Applications
From the world of nanotechnology we’ve gotten electronic skin, or e-skin, and electronic eye implants or e-eyes. Now we’re on the verge of electronic whiskers. Researchers with Berkeley Lab and the University of California (UC) Berkeley have created tactile sensors from composite films of carbon nanotubes and silver nanoparticles similar to the highly sensitive whiskers of cats and rats. These new e-whiskers respond to pressure as slight as a single Pascal, about the pressure exerted on a table surface by a dollar bill. Among their many potential applications is giving robots new abilities to “see” and “feel” their surrounding environment.
“Whiskers are hair-like tactile sensors used by certain mammals and insects to monitor wind and navigate around obstacles in tight spaces,” says the leader of this research Ali Javey, a faculty scientist in Berkeley Lab’s Materials Sciences Division and a UC Berkeley professor of electrical engineering and computer science. “Our electronic whiskers consist of high-aspect-ratio elastic fibers coated with conductive composite films of nanotubes and nanoparticles. In tests, these whiskers were 10 times more sensitive to pressure than all previously reported capacitive or resistive pressure sensors.”
Javey and his research group have been leaders in the development of e-skin and other flexible electronic devices that can interface with the environment. In this latest effort, they used a carbon nanotube paste to form an electrically conductive network matrix with excellent bendability. To this carbon nanotube matrix they loaded a thin film of silver nanoparticles that endowed the matrix with high sensitivity to mechanical strain.
“The strain sensitivity and electrical resistivity of our composite film is readily tuned by changing the composition ratio of the carbon nanotubes and the silver nanoparticles,” Javey says. “The composite can then be painted or printed onto high-aspect-ratio elastic fibers to form e-whiskers that can be integrated with different user-interactive systems.”
Javey notes that the use of elastic fibers with a small spring constant as the structural component of the whiskers provides large deflection and therefore high strain in response to the smallest applied pressures. As proof-of-concept, he and his research group successfully used their e-whiskers to demonstrate highly accurate 2D and 3D mapping of wind flow. In the future, e-whiskers could be used to mediate tactile sensing for the spatial mapping of nearby objects, and could also lead to wearable sensors for measuring heartbeat and pulse rate.
“Our e-whiskers represent a new type of highly responsive tactile sensor networks for real time monitoring of environmental effects,” Javey says. “The ease of fabrication, light weight and excellent performance of our e-whiskers should have a wide range of applications for advanced robotics, human-machine user interfaces, and biological applications.”
A paper describing this research has been published in the Proceedings of the National Academy of Sciences. The paper is titled “Highly sensitive electronic whiskers based on patterned carbon nanotube and silver nanoparticle composite films.” Javey is the corresponding author. Co-authors are Kuniharu Takei, Zhibin Yu, Maxwell Zheng, Hiroki Ota and Toshitake Takahashi.
(Source: newscenter.lbl.gov)
Infections damage our ability to form spatial memories
Increased inflammation following an infection impairs the brain’s ability to form spatial memories – according to new research. The impairment results from a decrease in glucose metabolism in the brain’s memory centre, disrupting the neural circuits involved in learning and memory.
Inflammation has long been linked to disorders of memory like Alzheimer’s disease. Severe infections can also impair cognitive function in healthy elderly individuals. The new findings published in the journal Biological Psychiatry help explain why inflammation impairs memory and could spur the development of new drugs targeting the immune system to treat dementia.
In the first trial to image how inflammation impairs human memory, the team at Brighton and Sussex Medical School scanned 20 participants before and after either a benign salty water injection or typhoid vaccination, used to induce inflammation. Positron emission tomography (PET) was used to measure the effects of inflammation on the consumption of glucose in the brain and after each scan participants tested their spatial memory by performing a series of tasks in a virtual reality.
A reduction in glucose metabolism within the brain’s memory centre, known as the Medial Temporal Lobe (MTL), was seen following inflammation. Participants also performed less well in spatial memory tasks, an effect that appeared to be directly mediated by the change in MTL metabolism.
"We have known for some time that severe infections can lead to long-term cognitive impairment in the elderly. Infections are also a common trigger for acute decline in function in patients with dementia and Alzheimer’s disease," explains Dr Neil Harrison, a Wellcome Trust Intermediate Clinical Fellow at BSMS who led the study. "This study suggests that catching a cold or the flu, which leads to inflammation in the brain, could impair our memory."
Infections are unlikely to cause long-term detrimental impact in the young and healthy but the findings are of great significance in the elderly. The team now plan to investigate the role of inflammation in dementia, including insight into how acute infections such as influenza influence the rate of progression and decline.
"Our findings suggest that the brain’s memory circuits are particularly sensitive to inflammation and help clarify the association between inflammation and decline in dementia," says Dr Harrison. "If we can control levels of inflammation, we may be able to reduce the rate of decline in patients’ cognition."
(Source: eurekalert.org)
How Inactivity Changes the Brain
A number of studies have shown that exercise can remodel the brain by prompting the creation of new brain cells and inducing other changes. Now it appears that inactivity, too, can remodel the brain, according to a notable new report.
The study, which was conducted in rats but likely has implications for people too, the researchers say, found that being sedentary changes the shape of certain neurons in ways that significantly affect not just the brain but the heart as well. The findings may help to explain, in part, why a sedentary lifestyle is so bad for us.
Until about 20 years ago, most scientists believed that the brain’s structure was fixed by adulthood, that you couldn’t create new brain cells, alter the shape of those that existed or in any other way change your mind physically after adolescence.
But in the years since, neurological studies have established that the brain retains plasticity, or the capacity to be reshaped, throughout our lifetimes. Exercise appears to be particularly adept at remodeling the brain, studies showed.
But little has been known about whether inactivity likewise alters the structure of the brain and, if so, what the consequences might be.
So for a study recently published in The Journal of Comparative Neurology, scientists at Wayne State University School of Medicine and other institutions gathered a dozen rats. They settled half of them in cages with running wheels and let the animals run at will. Rats like running, and these animals were soon covering about three miles a day on their wheels.
The other rats were housed in cages without wheels and remained sedentary.
Highly Reliable Brain Imaging Protocol Identifies Delays in Premature Infants
Infants born prematurely are at elevated risk for cognitive, motor, and behavioral deficits — the severity of which was, until recently, almost impossible to accurately predict in the neonatal period with conventional brain imaging technology. But physicians may now be able to identify the premature infants most at risk for deficits as well as the type of deficit, enabling them to quickly initiate early neuroprotective therapies, by using highly reliable 3-D MRI imaging techniques developed by clinician scientists at The Research Institute at Nationwide Children’s Hospital. The imaging technique also facilitates early and repeatable assessments of these therapies to help clinicians and researchers determine whether neuroprotective treatments are effective in a matter of weeks, instead of the two to five years previously required.
The researchers — experts in brain imaging and anatomy — developed a protocol for using the special imaging technique to study the development of 10 brain tracts in these tiny patients, work published online January 24 in PLOS One. Colorful 3-D images of each tract revealed the connections of the segments to different parts of the brain or the spinal cord. Each of the 10 tracts is important for certain functions and abilities, such as language, movement or vision.
“Developing a reliable and reproducible methodology for studying the premature brain was crucial in order for us to get to the next step: assessing neuroprotective therapies,” said Nehal A. Parikh, DO, principal investigator in the Center for Perinatal Research at Nationwide Children’s and senior author on the paper. “Now that we have this protocol, we can improve the standard of care and evaluate efforts to promote brain health within 8 to 12 weeks of beginning the interventions. That way, we can quickly see what really works.”
The study tested a detailed approach to measuring brain structure in extremely low birth weight infants at term-equivalent age by comparing their diffusion tensor tractography (DTT) scans to those of healthy, full-term newborns. DTT is a special MRI technique that produces 3-D images and is able to detect the brain’s structure and more subtle injuries than earlier forms of the technology.
The research team is the first to confirm differences in the fibrous structure of the 10 tracts between healthy, full-term infant brains and those of premature babies. Although the imaging technology is regularly used in adults, the tiny head size and lack of benchmark measurements in healthy infants meant that the use of DTT in premature infants was previously uncharted territory. With the detailed technique developed by Dr. Parikh’s team, the images can now be reproducibly processed and reliably interpreted.
“This protocol opens the field to far greater use of the methodology for targeting and assessing therapies in these infants,” said Dr. Parikh, who also is an associate professor of pediatrics at The Ohio State University College of Medicine. “We already have studies underway using our DTT segmentation methodology to measure the effectiveness of early neuroprotective interventions, such as the use of breast milk or skin-to-skin contact while premature babies are in intensive care.”
As imaging technology continues to be refined, the goal of targeted therapies based on the specific region of the brain with a delay or injury will become reality, Dr. Parikh predicted.For example, if an infant’s DTT scan indicates an under-developed corticospinal tract — the region of the brain controlling motor ability — physicians could immediately begin proactive physical therapies with the baby instead of waiting until the delay manifests itself. A repeat DTT scan a few months after beginning the therapy could then detect whether the therapy is effectively improving the structure of that brain tract.
“Because cognitive and behavioral deficits cannot be diagnosed until school age, there is an urgent need for robust early prognostic biomarkers,” said Dr. Parikh. “Our work is an important step in this direction and will facilitate early testing of neuroprotective interventions.”
(Source: nationwidechildrens.org)
Can Fish Oil Help Preserve Brain Cells?
People with higher levels of the omega-3 fatty acids found in fish oil may also have larger brain volumes in old age equivalent to preserving one to two years of brain health, according to a study published in the January 22, 2014, online issue of Neurology®, the medical journal of the American Academy of Neurology. Shrinking brain volume is a sign of Alzheimer’s disease as well as normal aging.
For the study, the levels of omega-3 fatty acids EPA+DHA in red blood cells were tested in 1,111 women who were part of the Women’s Health Initiative Memory Study. Eight years later, when the women were an average age of 78, MRI scans were taken to measure their brain volume.
Those with higher levels of omega-3s had larger total brain volumes eight years later. Those with twice as high levels of fatty acids (7.5 vs. 3.4 percent) had a 0.7 percent larger brain volume.
“These higher levels of fatty acids can be achieved through diet and the use of supplements, and the results suggest that the effect on brain volume is the equivalent of delaying the normal loss of brain cells that comes with aging by one to two years,” said study author James V. Pottala, PhD, of the University of South Dakota in Sioux Falls and Health Diagnostic Laboratory, Inc., in Richmond, Va.
Those with higher levels of omega-3s also had a 2.7 percent larger volume in the hippocampus area of the brain, which plays an important role in memory. In Alzheimer’s disease, the hippocampus begins to atrophy even before symptoms appear.
Honesty beats dishonesty for making you feel good
A University of Toronto report based on two neural imaging studies that monitored brain activity has found a reward given for telling the truth gives people greater satisfaction than the same reward given for deceit.
These studies were published recently in the neuroscience journals Neuropsychologia and NeuroImage.
"Our findings together show that people typically find truth-telling to be more rewarding than lying in different types of deceptive situations,” said Professor Kang Lee,whose research is funded in part by the Social Sciences and Humanities Research Council.
The findings are based on two studies of Chinese participants using a new neuroimaging method called near-infrared spectroscopy. The studies are among the first to address the question of whether lying makes people feel better or worse than telling the truth.
The studies explored two different types of deception. In first-order deception, the recipient does not know the deceiver is lying. In second-order deception, the deceivers are fully aware that the recipient knows their intention, such as bluffing in poker.
The researchers were surprised to find that a liar’s cortical reward system was more active when a reward was gained through truth-telling than lying. This was true in both types of deception.
Researchers also found that in both types of deception, telling a lie produced greater brain activations than telling the truth in the frontal lobe, suggesting lying is cognitively more taxing than truth-telling and uses more neural resources.
The researchers hope this study will advance understanding of the neural mechanisms underlying lying, a ubiquitous and frequent human behaviour, and help to diagnose pathological liars who may have different neural responses when lying or telling the truth.
Aspirin Intake May Halt Growth of Vestibular Schwannomas/Acoustic Neuromas
Researchers from Massachusetts Eye and Ear, Harvard Medical School, Massachusetts Institute of Technology and Massachusetts General Hospital have demonstrated, for the first time, that aspirin intake correlates with halted growth of vestibular schwannomas (also known as acoustic neuromas), a sometimes lethal intracranial tumor that typically causes hearing loss and tinnitus.
Image credit: Stanford School of Medicine/Oghalai Lab
Motivated by experiments in the Molecular Neurotology Laboratory at Mass. Eye and Ear involving human tumor specimens, the researchers performed a retrospective analysis of over 600 people diagnosed with vestibular schwannoma at Mass. Eye and Ear. Their research suggests the potential therapeutic role of aspirin in inhibiting tumor growth and motivates a clinical prospective study to assess efficacy of this well-tolerated anti-inflammatory medication in preventing growth of these intracranial tumors.
“Currently, there are no FDA-approved drug therapies to treat these tumors, which are the most common tumors of the cerebellopontine angle and the fourth most common intracranial tumors,” explains Konstantina Stankovic, M.D., Ph.D., who led the study. “Current options for management of growing vestibular schwannomas include surgery (via craniotomy) or radiation therapy, both of which are associated with potentially serious complications.”
The findings, which are described in the February issue of the journal Otology & Neurotology, were based on a retrospective series of 689 people, 347 of whom were followed with multiple magnetic resonance imaging MRI scans (50.3%). The main outcome measures were patient use of aspirin and rate of vestibular schwannoma growth measured by changes in the largest tumor dimension as noted on serial MRIs. A significant inverse association was found among aspirin users and vestibular schwannoma growth (odds ratio: 0.50, 95 percent confidence interval: 0.29-0.85), which was not confounded by age or gender.
“Our results suggest a potential therapeutic role of aspirin in inhibiting vestibular schwannoma growth,” said Dr. Stankovic, who is an otologic surgeon and researcher at Mass. Eye and Ear, Assistant Professor of Otology and Laryngology, Harvard Medical School (HMS), and member of the faculty of Harvard’s Program in Speech and Hearing Bioscience and Technology.
(Source: masseyeandear.org)
A time for memories
Neuroscientists from the University of Leicester, in collaboration with the Department of Neurosurgery at the University California Los Angeles (UCLA), are to reveal details of how the brain determines the timing at which neurons in specific areas fire to create new memories.
This research exploits the unique opportunity of recording multiple single-neurons in patients suffering from epilepsy refractory to medication that are implanted with intracranial electrodes for clinical reasons.
The study, which is to be published in the academic journal Current Biology, is the result of collaboration between Professor Rodrigo Quian Quiroga and Dr Hernan Rey at the Centre for Systems Neuroscience at the University of Leicester and Professor Itzhak Fried at UCLA.
The work follows up on the group’s research into what was dubbed the ‘Jennifer Aniston neurons’ – neurons in the hippocampus and its surrounding areas within the brain that specifically fire in an ‘abstract’ manner when we see or hear a certain concept - such as a person, an animal or a landscape - that we recognise.
Professor Quian Quiroga said: “The firing of these neurons is relatively very late after the moment of seeing the picture, or hearing the person’s name, but is still very precise. These neurons also fire only when the pictures are consciously recognised and remain silent when they are not.
“Our research shows that there is a specific brain response that marks the timing of the firing of these neurons. This response shortly precedes the neuron’s firing and is only present for the consciously recognised pictures - being absent if the pictures were not recognised.
“This brain response thus reflects an activation that provides a temporal window for processing consciously perceived stimuli in the hippocampus and surrounding cortex. Given the proposed role of these neurons in memory formation, we argue that the brain response we found is a gateway for processing consciously perceived stimuli to form or recall memories.”
Dr Hernan Rey, first author of the study, added: “This time-keeping may indeed be critical for synchronizing and combining multisensory information involving different processing times. This, in turn, helps in creating a unified conceptual representation that can be used for memory functions.”
Professor Quian Quiroga’s work is specifically concerned with examining how information about the external world - what we see, hear and touch - is represented by neurons in the brain and how this leads to the creation of our own internal representations and memories.
For example, we can easily recognize a person in a fraction of a second, even when seen from different angles, with different sizes, colours, contrasts and under strikingly different conditions. But how neurons in the brain are capable of creating such an ‘abstract’ representation, disregarding basic visual details, is only starting to be known.
(Source: www2.le.ac.uk)
Image caption: MMP-9 controls onset of paralysis in ALS mice. Sections of muscle stained for nerve (green) and muscle (red); nerve-muscle contacts appear yellow. In the SOD1 mouse, muscles that move the eye (left) retain nerve contacts and are active. Fast leg muscles (center) in the same animal lose nerve contacts (red stain only) and become paralyzed. Fast muscles from which MMP-9 has been genetically removed (right) retain their nerve contacts, and therefore muscle function, for nearly 3 months longer. This suggests that inhibiting MMP-9 in human patients with ALS should be beneficial. Credit: The Henderson Lab/Columbia University Medical Center.
Study Identifies Gene Tied to Motor Neuron Loss in ALS
Columbia University Medical Center (CUMC) researchers have identified a gene, called matrix metalloproteinase-9 (MMP-9), that appears to play a major role in motor neuron degeneration in amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease. The findings, made in mice, explain why most but not all motor neurons are affected by the disease and identify a potential therapeutic target for this still-incurable neurodegenerative disease. The study was published today in the online edition of the journal Neuron.
“One of the most striking aspects of ALS is that some motor neurons—specifically, those that control eye movement and eliminative and sexual functions—remain relatively unimpaired in the disease,” said study leader Christopher E. Henderson, PhD, the Gurewitsch and Vidda Foundation Professor of Rehabilitation and Regenerative Medicine, professor of pathology & cell biology and neuroscience (in neurology), and co-director of Columbia’s Motor Neuron Center. “We thought that if we could find out why these neurons have a natural resistance to ALS, we might be able to exploit this property and develop new therapeutic options.”
To understand why only some motor neurons are vulnerable to ALS, the researchers used DNA microarray profiling to compare the activity of tens of thousands of genes in neurons that resist ALS (oculomotor neurons/eye movement and Onuf’s nuclei/continence) with neurons affected by ALS (lumbar 5 spinal neurons/leg movement). The neurons were taken from normal mice.
“We found a number of candidate ‘susceptibility’ genes—genes that were expressed only in vulnerable motor neurons. One of those genes, MMP-9, was strongly expressed into adulthood. That was significant, as ALS is an adult-onset disease,” said co-lead author Krista J. Spiller, a former graduate student in Dr. Henderson’s laboratory who is now a postdoctoral fellow at the University of Pennsylvania. The other co-lead author is Artem Kaplan, a former MD-PhD student in the lab who is now a neurology resident at NewYork-Presbyterian Hospital/Columbia University Medical Center.
In a follow-up experiment, the researchers confirmed that the product of MMP-9, MMP-9 protein, is present in ALS-vulnerable motor neurons, but not in ALS-resistant ones. Further, the researchers found that MMP-9 can be detected not just in lumbar 5 neurons, but also in other types of motor neurons affected by ALS. “It was a perfect correlation.” said Dr. Henderson. “In other words, having MMP-9 is an absolute predictor that a motor neuron will die if the disease strikes, at least in mice.”
Taking a closer look at the groups of vulnerable motor neurons, the researchers found differences in MMP-9 expression at the single-cell level. Fast-fatigable neurons (which are involved in movements like jumping and sprinting and are the first to die in ALS) were found to have the most MMP-9 protein, whereas slow neurons (which control posture and are only partially affected in ALS) had none. “So, MMP-9 is not only labeling the most vulnerable groups of motor neurons, it is labeling the most vulnerable subtypes within those groups, as well,” said Dr. Spiller.
In another experiment, the researchers tested whether MMP-9 has afunctional role in ALS by crossing MMP-9 knockout mice with SOD1 mutant mice (a standard mouse model of ALS). Progeny from this cross with no MMP-9 exhibited an 80-day delay in loss of fast-fatigable motor neuron function and a 25 percent longer lifespan, compared with littermates with two copies of the MMP-9 gene. “This effect on nerve-muscle synapses is the largest ever seen in a mouse model of ALS,” said Dr. Spiller.
The same effect on motor neuron function was seen when MMP-9 was inactivated in SOD1 mutant mice using chemical injections or virally mediated gene therapy.
“Even after treatment, these mice didn’t have a normal lifespan, so inactivating MMP-9 is not a cure,” said Dr. Henderson. “But it’s remarkable that lowering levels of a single gene could have such a strong effect on the disease. That’s encouraging for therapeutic purposes.”
The researchers are still investigating how MMP-9 affects motor neuron function. Their findings suggest that the protein plays a role in increasing stress on the endoplasmic reticulum, an organelle involved in transporting and processing materials within cells. “Our goal is to learn more about MMP-9 and related pathways and to identify a new set of therapeutic targets,” said Dr. Henderson.
Brain Uses Serotonin To Perpetuate Chronic Pain Signals In Local Nerves
Setting the stage for possible advances in pain treatment, researchers at The Johns Hopkins University and the University of Maryland report they have pinpointed two molecules involved in perpetuating chronic pain in mice. The molecules, they say, also appear to have a role in the phenomenon that causes uninjured areas of the body to be more sensitive to pain when an area nearby has been hurt. A summary of the research will be published on Jan. 23 in the journal Neuron.
Image caption: Nerves in mouse skin that are actively responding to the painful stimulus capsaicin have been genetically engineered to glow green. Hairs appear in yellow. Credit: David Rini
"With the identification of these molecules, we have some additional targets that we can try to block to decrease chronic pain," says Xinzhong Dong, Ph.D., associate professor of neuroscience at the Johns Hopkins University School of Medicine and an early career scientist at Howard Hughes Medical Institute. "We found that persistent pain doesn’t always originate in the brain, as some had believed, which is important information for designing less addictive drugs to fight it."
Chronic pain that persists for weeks, months or years after an underlying injury or condition is resolved afflicts an estimated 20 to 25 percent of the population worldwide and about 116 million people in the U.S., costing Americans a total of $600 billion in medical interventions and lost productivity. It can be caused by everything from nerve injuries and osteoarthritis to cancer and stress.
In their new research, the scientists focused on a system of pain-sensing nerves within the faces of mice, known collectively as the trigeminal nerve. The trigeminal nerve is a large bundle of tens of thousands of nerve cells. Each cell is a long “wire” with a hub at its center; the hubs are grouped together into a larger hub. On one side of this hub, three smaller bundles of wires — V1, V2 and V3 — branch off. Each bundle contains individual pain-sensing wires that split off to cover a specific territory of the face. Signals are sent through the wires to the hubs of the cells and then travel to the spinal cord through a separate set of bundles. From the spinal cord, the signals are relayed to the brain, which interprets them as pain.
When the researchers pinched the V2 branch of the trigeminal nerve for a prolonged period of time, they found that the V2 and V3 territories were extra sensitive to additional pain. This spreading of pain to uninjured areas is typical of those experiencing chronic pain, but it can also be experienced during acute injuries, as when a thumb is hit with a hammer and the whole hand throbs with pain.
To figure out why, the researchers studied pain-sensing nerves in the skin of mouse ears. The smaller branches of the trigeminal V3 reach up into the skin of the lower ear. But an entirely different set of nerves is responsible for the skin of the upper ear. This distinction allowed the researchers to compare the responses of two unrelated groups of nerves that are in close proximity to each other.
To overcome the difficulty of monitoring nerve responses, Dong’s team inserted a gene into the DNA of mice so that the primary sensory nerve cells would glow green when activated. The pain-sensing nerves of the face are a subset of these.
When skin patches were then bathed in a dose of capsaicin — the active ingredient in hot peppers — the pain-sensing nerves lit up in both regions of the ear. But the V3 nerves in the lower ear were much brighter than those of the upper ear. The researchers concluded that pinching the connected-but-separate V2 branch of the trigeminal nerve had somehow sensitized the V3 nerves to “overreact” to the same amount of stimulus. (Watch nerves light up in this video.)
Applying capsaicin again to different areas, the researchers found that more nerve branches coming from a pinched V2 nerve lit up than those coming from an uninjured one. This suggests that nerves that don’t normally respond to pain can modify themselves during prolonged injury, adding to the pain signals being sent to the brain.
Knowing from previous studies that the protein TRPV1 is needed to activate pain-sensing nerve cells, the researchers next looked at its activity in the trigeminal nerve. They showed it was hyperactive in injured V2 nerve branches and in uninjured V3 branches, as well as in the branches that extended beyond the hub of the trigeminal nerve cell and into the spinal cord.
Next, University of Maryland experts in the neurological signaling molecule serotonin, aware that serotonin is involved in chronic pain, investigated its role in the TRPV1 activation study. The team, led by Feng Wei, M.D., Ph.D., blocked the production of serotonin, which is released from the brain stem into the spinal cord, and found that TRPV1 hyperactivity nearly disappeared.
Says Dong: “Chronic pain seems to cause serotonin to be released by the brain into the spinal cord. There, it acts on the trigeminal nerve at large, making TRPV1 hyperactive throughout its branches, even causing some non-pain-sensing nerve cells to start responding to pain. Hyperactive TRPV1 causes the nerves to fire more frequently, sending additional pain signals to the brain.”