Neuroscience

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Posts tagged neuron

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Brain rhythms help sense of location

Scientists have shed light on how mechanisms in the brain work to give us a sense of location. Research at the University of Edinburgh tracked electrical signals in the part of the brain linked to spatial awareness.

Sense of where we are

The study could help us understand how, if we know a room, we can go into it with our eyes shut and find our way around. This is closely related to the way we map out how to get from one place to another.

Brain’s electrical activity

Scientists found that brain cells, which code location through increases in electrical activity, do not do so by talking directly to each other. Instead, they can only send each other signals through cells that are known to reduce electrical activity. This is unexpected as cells that reduce electrical signalling are often thought to simply supress brain activity.

Rhythms of brain activity

The research also looked at electrical rhythms or waves of brain activity. Previous studies have found that spatial awareness is linked to not only the number and strength of electrical signals but also where on the electrical wave they occur.

The research shows that the indirect communication between nerve cells that are involved in spatial awareness also helps to explain how these electrical waves are generated. This finding is surprising because its suggests that the same cellular mechanisms allow our brains to work out our location and generate rhythmic waves of activity.

Spatial awareness and the brain’s electrical rhythms are known to be affected in conditions such as schizophrenia and Alzheimer’s disease. The scientists work could therefore help research in these areas.

Research

The study, funded by the Biotechnology and Biological Research Council, is published in the journal Neuron.

It looked at connections between nerve cells in the brain needed for spatial awareness in mice and then used computer modelling to recreate patterns of neural activity found in the brain.

Rhythms in brain activity are very mysterious and the research helps shed some light on this area as well as helping us understand how our brains code spatial information. It is particularly interesting that cells thought to encode location do not signal to each other directly but do so through intermediary cells. This is somewhat like members of a team not talking to each other, but instead sending messages via members of an opposing side. -Matt Nolan (Centre for Integrative Physiology)

(Source: ed.ac.uk)

Filed under brain cells brain activity spatial awareness neural activity neuron neuroscience science

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Potential Drug Target to Block Cell Death in Parkinson’s Disease Oxidative stress is a primary villain in a host of diseases that range from cancer and heart failure to Alzheimer’s disease, Amyotrophic Lateral Sclerosis and Parkinson’s disease. Now, scientists from the Florida campus of The Scripps Research Institute (TSRI) have found that blocking the interaction of a critical enzyme may counteract the destruction of neurons associated with these neurodegenerative diseases, suggesting a potential new target for drug development. These findings appear in the January 11, 2013 edition of The Journal of Biological Chemistry. During periods of cellular stress, such as exposure to UV radiation, the number of highly reactive oxygen-containing molecules can increase in cells, resulting in serious damage. However, relatively little is known about the role played in this process by a number of stress-related enzymes. In the new study, the TSRI team led by Professor Philip LoGrasso focused on an enzyme known as c-jun-N-terminal kinase (JNK). Under stress, JNK migrates to the mitochondria, the part of the cell that generates chemical energy and is involved in cell growth and death. That migration, coupled with JNK activation, is associated with a number of serious health issues, including mitochondrial dysfunction, which has long been known to contribute to neuronal death in Parkinson’s disease.  The new study showed for the first time that the interaction of JNK with a protein known as Sab is responsible for the initial JNK localization to the mitochondria in neurons. The scientists also found blocking JNK mitochondrial signaling by inhibiting JNK interaction with Sab can protect against neuronal damage in both cell culture and in the brain. In addition, by treating JNK with a peptide inhibitor derived from a mitochondrial membrane protein, the team was able to induce a two-fold level of protection of neurons in the substantia nigra pars compacta, the brain region devastated by Parkinson’s disease. The study noted that this inhibition leaves all other cell signaling intact, which could mean potentially fewer side effects in any future therapies. “This may be a novel way to prevent neuron degeneration,” said LoGrasso. “Now we can try to make compounds that block that translocation and see if they’re therapeutically viable.”

Potential Drug Target to Block Cell Death in Parkinson’s Disease

Oxidative stress is a primary villain in a host of diseases that range from cancer and heart failure to Alzheimer’s disease, Amyotrophic Lateral Sclerosis and Parkinson’s disease. Now, scientists from the Florida campus of The Scripps Research Institute (TSRI) have found that blocking the interaction of a critical enzyme may counteract the destruction of neurons associated with these neurodegenerative diseases, suggesting a potential new target for drug development.

These findings appear in the January 11, 2013 edition of The Journal of Biological Chemistry.

During periods of cellular stress, such as exposure to UV radiation, the number of highly reactive oxygen-containing molecules can increase in cells, resulting in serious damage. However, relatively little is known about the role played in this process by a number of stress-related enzymes.

In the new study, the TSRI team led by Professor Philip LoGrasso focused on an enzyme known as c-jun-N-terminal kinase (JNK). Under stress, JNK migrates to the mitochondria, the part of the cell that generates chemical energy and is involved in cell growth and death. That migration, coupled with JNK activation, is associated with a number of serious health issues, including mitochondrial dysfunction, which has long been known to contribute to neuronal death in Parkinson’s disease. 

The new study showed for the first time that the interaction of JNK with a protein known as Sab is responsible for the initial JNK localization to the mitochondria in neurons. The scientists also found blocking JNK mitochondrial signaling by inhibiting JNK interaction with Sab can protect against neuronal damage in both cell culture and in the brain.

In addition, by treating JNK with a peptide inhibitor derived from a mitochondrial membrane protein, the team was able to induce a two-fold level of protection of neurons in the substantia nigra pars compacta, the brain region devastated by Parkinson’s disease.

The study noted that this inhibition leaves all other cell signaling intact, which could mean potentially fewer side effects in any future therapies.

“This may be a novel way to prevent neuron degeneration,” said LoGrasso. “Now we can try to make compounds that block that translocation and see if they’re therapeutically viable.”

Filed under neurodegenerative diseases drug development neuron neuronal death science

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Study: Model for Brain Signaling Flawed A new study out today in the journal Science turns two decades of understanding about how brain cells communicate on its head. The study demonstrates that the tripartite synapse – a model long accepted by the scientific community and one in which multiple cells collaborate to move signals in the central nervous system – does not exist in the adult brain.  “Our findings demonstrate that the tripartite synaptic model is incorrect,” said Maiken Nedergaard, M.D., D.M.Sc., lead author of the study and co-director of the University of Rochester Medical Center (URMC) Center for Translational Neuromedicine. “This concept does not represent the process for transmitting signals between neurons in the brain beyond the developmental stage.” The central nervous system is home to many different cells. While neurons tend to garner the most attention, it is only recently that the function of the brain’s other cells have been fully appreciated. Glial cells known as astrocytes, for example, had long been considered mainly the “glue” that helps hold all the other cells in the central nervous system in place. Scientists now understand that that these cells are essential to maintaining a healthy environment in the brain by helping carry out functions such as removing waste. “Neurons are like a racing car,” said Nedergaard. “While the driver gets all the credit, there are often 20 people behind the scenes that are optimizing his or her success.” However, when it comes to moving signals between neurons in the brain it turns out that the scientists may have vastly exaggerated the role of the astrocyte.    Neurons are connected to each other via axons or “arms” that extend from the cell’s main body. Communication between neighboring neurons takes place where axons meet other nerve cells – called a synaptic juncture – when an electrical charge causes chemicals called neurotransmitters or glutamate to be released by one cell and “read” by receptors on the surface of the opposite. The two cells do not actually touch, so the chemicals messages must pass through a gap in the synaptic juncture. The space around this gap is insulated by astrocytes.    Under the tripartite synapse model, both astrocytes and neurons were believed to play a role in the “conversation” between cells. This understanding was largely based on animal models which showed active receptors and neurotransmission between not only the nerve cells but also the nearby astrocytes.   Specifically, a key neurotransmission receptor called metabotropic glutamate receptor 5 (mGluR5) was observed to be present and active in astrocytes at the synaptic juncture. It was also observed that when the mGluR5 receptor was activated, the astrocytes would release chemical transmitters that were in turn read by the nerve cells. These findings led to the conclusion that astrocytes must in some manner modulate the signaling process between brain cells.  While this model has held sway for decades, scientists have long been frustrated by their inability to influence this process by targeting it with drugs. “If this concept was correct, it should have given rise to a clinical trial by now,” said Nedergaard. “It has not, which tells us that with so many labs work on this for 20 years that there must be something wrong.” One of the barriers to understanding precise mechanics of passing signals from one neuron to another has been the inability to observe this process in the adult brain. The tripartite synapse model was based – in part – by examining the activity in the brains of very young rodents. Adult rodents could not be similarly studied because the synapses in the brain would die before they could be fully analyzed. This ultimately led to the presumption that the signaling process that was witnessed in the young brain carried over to adulthood.  Collaborating with researchers at the University of Rochester’s Institute of Optics, Nedergaard and her team developed a new 2-photon microscope that enables researchers to observe glia activity in the living brain. Using both this method and by analyzing the gene and protein expression in the brain the researchers discovered that the mGluR5 largely disappear in the glial cells of adult mice meaning that these cells do not directly respond to synaptic neuronal signalling, thus calling into question the concepts that drive most of ongoing research in the field. “The process of neuron-glial transmission as conceived by the tripartite synapse model appears to just be a simplistic signaling pathway that ‘teaches’ the synapse how to behave,” said Nedergaard. “Once the brain matures, it goes away.”

Study: Model for Brain Signaling Flawed

A new study out today in the journal Science turns two decades of understanding about how brain cells communicate on its head. The study demonstrates that the tripartite synapse – a model long accepted by the scientific community and one in which multiple cells collaborate to move signals in the central nervous system – does not exist in the adult brain. 

“Our findings demonstrate that the tripartite synaptic model is incorrect,” said Maiken Nedergaard, M.D., D.M.Sc., lead author of the study and co-director of the University of Rochester Medical Center (URMC) Center for Translational Neuromedicine. “This concept does not represent the process for transmitting signals between neurons in the brain beyond the developmental stage.”

The central nervous system is home to many different cells. While neurons tend to garner the most attention, it is only recently that the function of the brain’s other cells have been fully appreciated. Glial cells known as astrocytes, for example, had long been considered mainly the “glue” that helps hold all the other cells in the central nervous system in place. Scientists now understand that that these cells are essential to maintaining a healthy environment in the brain by helping carry out functions such as removing waste.

“Neurons are like a racing car,” said Nedergaard. “While the driver gets all the credit, there are often 20 people behind the scenes that are optimizing his or her success.”

However, when it comes to moving signals between neurons in the brain it turns out that the scientists may have vastly exaggerated the role of the astrocyte.   

Neurons are connected to each other via axons or “arms” that extend from the cell’s main body. Communication between neighboring neurons takes place where axons meet other nerve cells – called a synaptic juncture – when an electrical charge causes chemicals called neurotransmitters or glutamate to be released by one cell and “read” by receptors on the surface of the opposite. The two cells do not actually touch, so the chemicals messages must pass through a gap in the synaptic juncture. The space around this gap is insulated by astrocytes.   

Under the tripartite synapse model, both astrocytes and neurons were believed to play a role in the “conversation” between cells. This understanding was largely based on animal models which showed active receptors and neurotransmission between not only the nerve cells but also the nearby astrocytes.  

Specifically, a key neurotransmission receptor called metabotropic glutamate receptor 5 (mGluR5) was observed to be present and active in astrocytes at the synaptic juncture. It was also observed that when the mGluR5 receptor was activated, the astrocytes would release chemical transmitters that were in turn read by the nerve cells. These findings led to the conclusion that astrocytes must in some manner modulate the signaling process between brain cells. 

While this model has held sway for decades, scientists have long been frustrated by their inability to influence this process by targeting it with drugs.

“If this concept was correct, it should have given rise to a clinical trial by now,” said Nedergaard. “It has not, which tells us that with so many labs work on this for 20 years that there must be something wrong.”

One of the barriers to understanding precise mechanics of passing signals from one neuron to another has been the inability to observe this process in the adult brain. The tripartite synapse model was based – in part – by examining the activity in the brains of very young rodents. Adult rodents could not be similarly studied because the synapses in the brain would die before they could be fully analyzed. This ultimately led to the presumption that the signaling process that was witnessed in the young brain carried over to adulthood. 

Collaborating with researchers at the University of Rochester’s Institute of Optics, Nedergaard and her team developed a new 2-photon microscope that enables researchers to observe glia activity in the living brain. Using both this method and by analyzing the gene and protein expression in the brain the researchers discovered that the mGluR5 largely disappear in the glial cells of adult mice meaning that these cells do not directly respond to synaptic neuronal signalling, thus calling into question the concepts that drive most of ongoing research in the field.

“The process of neuron-glial transmission as conceived by the tripartite synapse model appears to just be a simplistic signaling pathway that ‘teaches’ the synapse how to behave,” said Nedergaard. “Once the brain matures, it goes away.”

Filed under tripartite synaptic model brain cells nerve cells nervous system neuron neuroscience science

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Newly found ‘volume control’ in the brain promotes learning, memory

Scientists have long wondered how nerve cell activity in the brain’s hippocampus, the epicenter for learning and memory, is controlled — too much synaptic communication between neurons can trigger a seizure, and too little impairs information processing, promoting neurodegeneration. Researchers at Georgetown University Medical Center say they now have an answer. In the January 10 issue of Neuron, they report that synapses that link two different groups of nerve cells in the hippocampus serve as a kind of “volume control,” keeping neuronal activity throughout that region at a steady, optimal level.

"Think of these special synapses like the fingers of God and man touching in Michelangelo’s famous fresco in the Sistine Chapel," says the study’s senior investigator, Daniel Pak, PhD, an associate professor of pharmacology. "Now substitute the figures for two different groups of neurons that need to perform smoothly. The touching of the fingers, or synapses, controls activity levels of neurons within the hippocampus."

The hippocampus is a processing unit that receives input from the cortex and consolidates that information in terms of learning and memory. Neurons known as granule cells, located in the hippocampus’ dentate gyrus, receive transmissions from the cortex. Those granule cells then pass that information to the other set of neurons (those in the CA3 region of the hippocampus, in this study) via the synaptic fingers.

Those fingers dial up, or dial down, the volume of neurotransmission from the granule cells to the CA3 region to keep neurotransmission in the learning and memory areas of the hippocampus at an optimal flow — a concept known as homeostatic plasticity. “If granule cells try to transmit too much activity, we found, the synaptic junction tamps down the volume of transmission by weakening their connections, allowing the proper amount of information to travel to CA3 neurons,” says Pak. “If there is not enough activity being transmitted by the granule cells, the synapses become stronger, pumping up the volume to CA3 so that information flow remains constant.”

There are many such touching fingers in the hippocampus, connecting the so-called “mossy fibers” of the granule cells to neurons in the CA3 region. But importantly, not every one of the billions of neurons in the hippocampus needs to set its own level of transmission from one nerve cell to the other, says Pak.

To explain, he uses another analogy. “It had previously been thought that neurons act separately like cars, each working to keep their speed at a constant level even though signal traffic may be fast or slow. But we wondered how these neurons could process learning and memory information efficiently, while also regulating the speed by which they process and communicate that information.

"We believe, based on our study, that only the mossy fiber synapses on the CA3 neurons control the level of activity for the hippocampus — they are like the engine on a train that sets the speed for all the other cars, or neurons, attached to it," Pak says. "That frees up the other neurons to do the job they are tasked with doing — processing and encoding information in the forms of learning and memory."

Not only does the study offer a new model for how homeostatic plasticity in the hippocampus can co-exist with learning and memory, it also suggests a new therapeutic avenue to help patients with uncontrollable seizures, he says.

"The CA3 region is highly susceptible to seizures, so if we understand how homeostasis is maintained in these neurons, we could potentially manipulate the system. When there is an excessive level of CA3 neuronal activity in a patient, we could learn how to therapeutically turn it down."

(Source: eurekalert.org)

Filed under learning memory neurotransmission nerve cells neuronal activity neuron neuroscience science

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Pesticides and Parkinson’s: UCLA researchers uncover further proof of a link For several years, neurologists at UCLA have been building a case that a link exists between pesticides and Parkinson’s disease. To date, paraquat, maneb and ziram — common chemicals sprayed in California’s Central Valley and elsewhere — have been tied to increases in the disease, not only among farmworkers but in individuals who simply lived or worked near fields and likely inhaled drifting particles. Now, UCLA researchers have discovered a link between Parkinson’s and another pesticide, benomyl, whose toxicological effects still linger some 10 years after the chemical was banned by the U.S. Environmental Protection Agency. Even more significantly, the research suggests that the damaging series of events set in motion by benomyl may also occur in people with Parkinson’s disease who were never exposed to the pesticide, according to Jeff Bronstein, senior author of the study and a professor of neurology at UCLA, and his colleagues. Benomyl exposure, they say, starts a cascade of cellular events that may lead to Parkinson’s. The pesticide prevents an enzyme called ALDH (aldehyde dehydrogenase) from keeping a lid on DOPAL, a toxin that naturally occurs in the brain. When left unchecked by ALDH, DOPAL accumulates, damages neurons and increases an individual’s risk of developing Parkinson’s. The investigators believe their findings concerning benomyl may be generalized to all Parkinson’s patients. Developing new drugs to protect ALDH activity, they say, may eventually help slow the progression of the disease, whether or not an individual has been exposed to pesticides. The research is published in the current online edition of Proceedings of the National Academy of Sciences.

Pesticides and Parkinson’s: UCLA researchers uncover further proof of a link

For several years, neurologists at UCLA have been building a case that a link exists between pesticides and Parkinson’s disease. To date, paraquat, maneb and ziram — common chemicals sprayed in California’s Central Valley and elsewhere — have been tied to increases in the disease, not only among farmworkers but in individuals who simply lived or worked near fields and likely inhaled drifting particles.

Now, UCLA researchers have discovered a link between Parkinson’s and another pesticide, benomyl, whose toxicological effects still linger some 10 years after the chemical was banned by the U.S. Environmental Protection Agency.

Even more significantly, the research suggests that the damaging series of events set in motion by benomyl may also occur in people with Parkinson’s disease who were never exposed to the pesticide, according to Jeff Bronstein, senior author of the study and a professor of neurology at UCLA, and his colleagues.

Benomyl exposure, they say, starts a cascade of cellular events that may lead to Parkinson’s. The pesticide prevents an enzyme called ALDH (aldehyde dehydrogenase) from keeping a lid on DOPAL, a toxin that naturally occurs in the brain. When left unchecked by ALDH, DOPAL accumulates, damages neurons and increases an individual’s risk of developing Parkinson’s.

The investigators believe their findings concerning benomyl may be generalized to all Parkinson’s patients. Developing new drugs to protect ALDH activity, they say, may eventually help slow the progression of the disease, whether or not an individual has been exposed to pesticides.

The research is published in the current online edition of Proceedings of the National Academy of Sciences.

Filed under parkinson's disease pesticides benomyl brain neuron environment science

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Induction of adult cortical neurogenesis by an antidepressant

The production of new neurons in the adult normal cortex in response to the antidepressant, fluoxetine, is reported in a study published online this week in Neuropsychopharmacology.

The research team, which is based at the Institute for Comprehensive Medical Science, Fujita Health University, Aichi, has previously demonstrated that neural progenitor cells exist at the surface of the adult cortex, and, moreover, that ischemia enhances the generation of new inhibitory neurons from these neural progenitor cells. These cells were accordingly named “Layer 1 Inhibitory Neuron Progenitor cells” (L1-INP). However, until now it was not known whether L1-INP-related neurogenesis could be induced in the normal adult cortex.

Tsuyoshi Miyakawa, Koji Ohira, and their colleagues employed fluoxetine, a selective serotonin reuptake inhibitor, and one of the most widely used antidepressants, to stimulate the production of new neurons from L1-INP cells. A large percentage of these newly generated neurons were inhibitory GABAergic interneurons, and their generation coincided with a reduction in apoptotic cell death following ischemia. This finding highlights the potential neuroprotective response induced by this antidepressant drug. It also lends further support to the postulation that induction of adult neurogenesis in cortex is a relevant prevention/treatment option for neurodegenerative diseases and psychiatric disorders.

(Source: eurekalert.org)

Filed under neurogenesis fluoxetine neuron antidepressants interneurons neuroscience science

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The Nerve-Growth Factor: A New Tool for Manipulating Neurons The human nervous system is a vast network of several billion neurons, or nerve cells, endowed with the remarkable ability to receive, store and transmit information. In order to communicate with one another and with non-neuronal cells the neurons rely on the long extensions called axons, which are somewhat analogous to electrically conducting wires. Unlike wires, however, the axons are fluid-filled cylindrical structures that not only transmit electrical signals but also ferry nutrients and other essential substances to and from the cell body. Many basic questions remain to be answered about the mechanisms governing the formation of this intricate cellular network. How do the nerve cells differentiate into thousands of different types? How do their axons establish specific connections (synapses) with other neurons and non-neuronal cells? And what is the nature of the chemical messages neurons send and receive once the synaptic connections are made? This article will describe some major characteristics and effects of a protein called the nerve-growth factor (NGF), which has made it possible to induce and analyze under highly favorable conditions some crucial steps in the differentiation of neurons, such as the growth and maturation of axons and the synthesis and release of neurotransmitters: the bearers of the chemical messages. The discovery of NGF has also promoted an intensive search for other specific growth factors, leading to the isolation and characterization of a number of proteins with the ability to enhance the growth of different cell lines. Continue reading

The Nerve-Growth Factor: A New Tool for Manipulating Neurons

The human nervous system is a vast network of several billion neurons, or nerve cells, endowed with the remarkable ability to receive, store and transmit information. In order to communicate with one another and with non-neuronal cells the neurons rely on the long extensions called axons, which are somewhat analogous to electrically conducting wires. Unlike wires, however, the axons are fluid-filled cylindrical structures that not only transmit electrical signals but also ferry nutrients and other essential substances to and from the cell body. Many basic questions remain to be answered about the mechanisms governing the formation of this intricate cellular network. How do the nerve cells differentiate into thousands of different types? How do their axons establish specific connections (synapses) with other neurons and non-neuronal cells? And what is the nature of the chemical messages neurons send and receive once the synaptic connections are made?

This article will describe some major characteristics and effects of a protein called the nerve-growth factor (NGF), which has made it possible to induce and analyze under highly favorable conditions some crucial steps in the differentiation of neurons, such as the growth and maturation of axons and the synthesis and release of neurotransmitters: the bearers of the chemical messages. The discovery of NGF has also promoted an intensive search for other specific growth factors, leading to the isolation and characterization of a number of proteins with the ability to enhance the growth of different cell lines.

Continue reading

Filed under nerve-growth factor nerve cells protein neuron neurotransmitters science

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Soma by the Flaming Lotus Girls translates the anatomy of neurons into metal, fire and light; magnifying the microscopic world to an epic scale. In Soma, an elegant axon arch connects an earthbound neuron with its partner floating overhead.

Soma is an interactive sculptural installation depicting two communicating neurons made of stainless steel, copper, aluminum, bronze, resin, fire and light. Each of Soma’s two neurons has a spinning fire nucleus. The nuclei are counter spinning balls of flame with variable speed motors.

Fire and light flow like electrochemical signals between Soma’s two neurons. Spinning balls of fire form the neuron’s nuclei. Slender dendrites extend to the sky and reach down to the earth, emitting constant flame and color changing light.

Soma is 25 feet high and 50 feet long. It is roughly a rectangular shape that occupies approximately 5,000 square feet including the fuel depot. She uses up to 100 gallons of fuel per hour.

There are 35 Dendrites using approx. 21’ of stainless steel tubing each. 735 feet of stainless steel tubing was used for dendrites over all.

Two dodecahedrons constructed from 24 stainless steel pentagons comprise the cell bodies of Soma, and enclose the nuclei. Each pentagon used about 10’ of stainless steel tubing. A total 240 feet of stainless steel tubing was used for the dodecahedrons.

There are flame effects running down the axon which simulate signal neurotransmission. Participants control the “neurotransmission” by pushing buttons. A “Sparkle Poof” simulates release of neurotransmitters at the synapse. Each aerial dendrite and the axon burn with continuous flame effects.


Filed under art dendrites neuron sculpture soma flaming lotus girls neuroscience science

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A new type of nerve cell found in the brain Scientists at Karolinska Institutet in Sweden, in collaboration with colleagues in Germany and the Netherlands, have identified a previously unknown group of nerve cells in the brain. The nerve cells regulate cardiovascular functions such as heart rhythm and blood pressure. It is hoped that the discovery, which is published in the Journal of Clinical Investigation, will be significant in the long term in the treatment of cardiovascular diseases in humans. The scientists have managed to identify in mice a previously totally unknown group of nerve cells in the brain. These nerve cells, also known as ‘neurons’, develop in the brain with the aid of thyroid hormone, which is produced in the thyroid gland. Patients in whom the function of the thyroid gland is disturbed and who therefore produce too much or too little thyroid hormone, thus risk developing problems with these nerve cells. This in turn has an effect on the function of the heart, leading to cardiovascular disease. It is well-known that patients with untreated hyperthyroidism (too high a production of thyroid hormone) or hypothyroidism (too low a production of thyroid hormone) often develop heart problems. It has previously been believed that this was solely a result of the hormone affecting the heart directly. The new study, however, shows that thyroid hormone also affects the heart indirectly, through the newly discovered neurons. "This discovery opens the possibility of a completely new way of combating cardiovascular disease", says Jens Mittag, group leader at the Department of Cell and Molecular Biology at Karolinska Institutet. "If we learn how to control these neurons, we will be able to treat certain cardiovascular problems like hypertension through the brain. This is, however, still far in the future. A more immediate conclusion is that it is of utmost importance to identify and treat pregnant women with hypothyroidism, since their low level of thyroid hormone may harm the production of these neurons in the foetus, and this may in the long run cause cardiovascular disorders in the offspring."

A new type of nerve cell found in the brain

Scientists at Karolinska Institutet in Sweden, in collaboration with colleagues in Germany and the Netherlands, have identified a previously unknown group of nerve cells in the brain. The nerve cells regulate cardiovascular functions such as heart rhythm and blood pressure. It is hoped that the discovery, which is published in the Journal of Clinical Investigation, will be significant in the long term in the treatment of cardiovascular diseases in humans.

The scientists have managed to identify in mice a previously totally unknown group of nerve cells in the brain. These nerve cells, also known as ‘neurons’, develop in the brain with the aid of thyroid hormone, which is produced in the thyroid gland. Patients in whom the function of the thyroid gland is disturbed and who therefore produce too much or too little thyroid hormone, thus risk developing problems with these nerve cells. This in turn has an effect on the function of the heart, leading to cardiovascular disease.

It is well-known that patients with untreated hyperthyroidism (too high a production of thyroid hormone) or hypothyroidism (too low a production of thyroid hormone) often develop heart problems. It has previously been believed that this was solely a result of the hormone affecting the heart directly. The new study, however, shows that thyroid hormone also affects the heart indirectly, through the newly discovered neurons.

"This discovery opens the possibility of a completely new way of combating cardiovascular disease", says Jens Mittag, group leader at the Department of Cell and Molecular Biology at Karolinska Institutet. "If we learn how to control these neurons, we will be able to treat certain cardiovascular problems like hypertension through the brain. This is, however, still far in the future. A more immediate conclusion is that it is of utmost importance to identify and treat pregnant women with hypothyroidism, since their low level of thyroid hormone may harm the production of these neurons in the foetus, and this may in the long run cause cardiovascular disorders in the offspring."

Filed under nerve cells heart cardiovascular disease thyroid thyroid hormone neuron neuroscience science

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