Neuroscience

Articles and news from the latest research reports.

Posts tagged science

164 notes

Will we ever… have cyborg brains?
For the first time in over 15 years, Cathy Hutchinson brought a coffee to her lips and smiled. Cathy had suffered from the paralysing effects of a stroke, but when neurosurgeons implanted tiny recording devices in her brain, she could use her thought patterns to guide a robot arm that delivered her hot drink. This week, it was reported that Jan Scheuermann, who is paralysed from the neck down, could grasp and move a variety of objects by controlling a robotic arm with her mind.
In both cases the implants convert brain signals into digital commands that a robotic device can follow. It’s a remarkable achievement, one that could transform the lives of people debilitated through illness.
Yet it’s still a far cry from the visions of man fused with machine, or cyborgs, that grace computer games or sci-fi. The dream is to create the type of brain augmentations we see in fiction that provide cyborgs with advantages or superhuman powers. But the ones being made in the lab only aim to restore lost functionality – whether it’s brain implants that restore limb control, or cochlear implants for hearing.
Creating implants that improve cognitive capabilities, such as an enhanced vision “gadget” that can be taken from a shelf and plugged into our brain, or implants that can restore or enhance brain function is understandably a much tougher task. But some research groups are being to make some inroads.
For instance, neuroscientists Matti Mintz from Tel Aviv University and Paul Verschure from Universitat Pompeu Fabra in Barcelona, Spain, are trying to develop an implantable chip that can restore lost movement through the ability to learn new motor functions, rather than regaining limb control. Verschure’s team has developed a mathematical model that mimics the flow of signals in the cerebellum, the region of the brain that plays an important role in movement control. The researchers programmed this model onto a circuit and connected it with electrodes to a rat’s brain. If they tried to teach the rat a conditioned motor reflex – to blink its eye when it sensed an air puff – while its cerebellum was “switched off” by being anaesthetised, it couldn’t respond. But when the team switched the chip on, this recorded the signal from the air puff, processed it, and sent electrical impulses to the rat’s motor neurons. The rat blinked, and the effect lasted even after it woke up.
Continue reading

Will we ever… have cyborg brains?

For the first time in over 15 years, Cathy Hutchinson brought a coffee to her lips and smiled. Cathy had suffered from the paralysing effects of a stroke, but when neurosurgeons implanted tiny recording devices in her brain, she could use her thought patterns to guide a robot arm that delivered her hot drink. This week, it was reported that Jan Scheuermann, who is paralysed from the neck down, could grasp and move a variety of objects by controlling a robotic arm with her mind.

In both cases the implants convert brain signals into digital commands that a robotic device can follow. It’s a remarkable achievement, one that could transform the lives of people debilitated through illness.

Yet it’s still a far cry from the visions of man fused with machine, or cyborgs, that grace computer games or sci-fi. The dream is to create the type of brain augmentations we see in fiction that provide cyborgs with advantages or superhuman powers. But the ones being made in the lab only aim to restore lost functionality – whether it’s brain implants that restore limb control, or cochlear implants for hearing.

Creating implants that improve cognitive capabilities, such as an enhanced vision “gadget” that can be taken from a shelf and plugged into our brain, or implants that can restore or enhance brain function is understandably a much tougher task. But some research groups are being to make some inroads.

For instance, neuroscientists Matti Mintz from Tel Aviv University and Paul Verschure from Universitat Pompeu Fabra in Barcelona, Spain, are trying to develop an implantable chip that can restore lost movement through the ability to learn new motor functions, rather than regaining limb control. Verschure’s team has developed a mathematical model that mimics the flow of signals in the cerebellum, the region of the brain that plays an important role in movement control. The researchers programmed this model onto a circuit and connected it with electrodes to a rat’s brain. If they tried to teach the rat a conditioned motor reflex – to blink its eye when it sensed an air puff – while its cerebellum was “switched off” by being anaesthetised, it couldn’t respond. But when the team switched the chip on, this recorded the signal from the air puff, processed it, and sent electrical impulses to the rat’s motor neurons. The rat blinked, and the effect lasted even after it woke up.

Continue reading

Filed under brain robotics prosthetics implants bionics neuroscience science

400 notes

Human hands have ‘evolved for fighting’

Compared with apes, humans have shorter palms and fingers and longer, stronger flexible thumbs. Experts have long assumed these features evolved to help our ancestors make and use tools. But new evidence from the US suggests it was not just dexterity that shaped the human hand, but violence also.


Hands largely evolved through natural selection to form a punching fist, it is claimed. ”The role aggression has played in our evolution has not been adequately appreciated,” said Professor David Carrier, from the University of Utah.
”There are people who do not like this idea but it is clear that compared with other mammals, great apes are a relatively aggressive group with lots of fighting and violence, and that includes us. We’re the poster children for violence.”
The forces of natural selection that drove hands to become nimble-fingered also turned them into weapons, Prof Carrier believes.
”Individuals who could strike with a clenched fish could hit harder without injuring themselves, so they were better able to fight for mates and thus be more likely to reproduce,” he said.
”If a fist posture does provide a performance advantage for punching, the proportions of our hands also may have evolved in response to selection for fighting ability, in addition to selection for dexterity.”

Human hands have ‘evolved for fighting’

Compared with apes, humans have shorter palms and fingers and longer, stronger flexible thumbs. Experts have long assumed these features evolved to help our ancestors make and use tools. But new evidence from the US suggests it was not just dexterity that shaped the human hand, but violence also.

Hands largely evolved through natural selection to form a punching fist, it is claimed. ”The role aggression has played in our evolution has not been adequately appreciated,” said Professor David Carrier, from the University of Utah.

”There are people who do not like this idea but it is clear that compared with other mammals, great apes are a relatively aggressive group with lots of fighting and violence, and that includes us. We’re the poster children for violence.”

The forces of natural selection that drove hands to become nimble-fingered also turned them into weapons, Prof Carrier believes.

”Individuals who could strike with a clenched fish could hit harder without injuring themselves, so they were better able to fight for mates and thus be more likely to reproduce,” he said.

”If a fist posture does provide a performance advantage for punching, the proportions of our hands also may have evolved in response to selection for fighting ability, in addition to selection for dexterity.”

Filed under evolution aggression natural selection science

46 notes

Transplanted neural stem cells treat ALS in mouse model
Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, is untreatable and fatal. Nerve cells in the spinal cord die, eventually taking away a person’s ability to move or even breathe. A consortium of ALS researchers at multiple institutions, including Sanford-Burnham Medical Research Institute, Brigham and Women’s Hospital, and the University of Massachusetts Medical School, tested transplanted neural stem cells as a treatment for the disease. In 11 independent studies, they found that transplanting neural stem cells into the spinal cord of a mouse model of ALS slows disease onset and progression. This treatment also improves host motor function and significantly prolongs survival.
Surprisingly, the transplanted neural stem cells did not benefit ALS mice by replacing deteriorating nerve cells. Instead, neural stem cells help by producing factors that preserve the health and function of the host’s remaining nerve cells. They also reduce inflammation and suppress the number of disease-causing cells in the host’s spinal cord. These findings, published December 19 in Science Translational Medicine, demonstrate the potential neural stem cells hold for treating ALS and other nervous system disorders.
“While not a cure for human ALS, we believe that the careful transplantation of neural stem cells, particularly into areas that can best sustain life—respiratory control centers, for example—may be ready for clinical trials,” Evan Y. Snyder, M.D., Ph.D., director of Sanford-Burnham’s Stem Cell and Regenerative Biology Program and senior author of the study.
Neural stem cells
In this study, researchers at multiple institutions conducted 11 independent studies to test neural stem cell transplantation in a well-established mouse model of ALS. They all found that this cell therapy reduced the symptoms and course of the ALS-like disease. They observed improved motor performance and respiratory function in treated mice. Neural stem cell transplant also slowed the disease’s progression. What’s more, 25 percent of the treated ALS mice in this study survived for one year or more—roughly three to four times longer than untreated mice.
Neural stem cells are the precursors of all brain cells. They can self-renew, making more neural stem cells, and differentiate, becoming nerve cells or other brain cells. These cells can also rescue malfunctioning nerve cells and help preserve and regenerate host brain tissue. But they’ve never before been studied extensively in a good model of adult ALS.
How neural stem cells benefit ALS mice
Transplanted neural stem cells helped the ALS mice, but not for the obvious reason—not because they became nerve cells, replacing those missing in the ALS spinal cord. The biggest impact actually came from a series of other beneficial neural stem cell activities. It turns out neural stem cells produce protective molecules. They also trigger host cells to produce their own protective molecules. In turn, these factors help spare host nerve cells from further destruction.
Then a number of other positive events take place in treated mice. The transplanted normal neural stem cells change the fate of the host’s own diseased neural stem cells—for the better. This change decreases the number of toxin-producing, disease-promoting cells in the host’s spinal cord. Transplanted neural stem cells also reduce inflammation.
“We discovered that cell replacement plays a surprisingly small role in these impressive clinical benefits. Rather, the stem cells change the host environment for the better and protect the endangered nerve cells,” said Snyder. “This realization is important because most diseases are now being recognized as multifaceted in their cause and their symptoms—they don’t involve just one cell type or one malfunctioning process. We are coming to recognize that the multifaceted actions of the stem cell may address a number of these disease processes.”

Transplanted neural stem cells treat ALS in mouse model

Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, is untreatable and fatal. Nerve cells in the spinal cord die, eventually taking away a person’s ability to move or even breathe. A consortium of ALS researchers at multiple institutions, including Sanford-Burnham Medical Research Institute, Brigham and Women’s Hospital, and the University of Massachusetts Medical School, tested transplanted neural stem cells as a treatment for the disease. In 11 independent studies, they found that transplanting neural stem cells into the spinal cord of a mouse model of ALS slows disease onset and progression. This treatment also improves host motor function and significantly prolongs survival.

Surprisingly, the transplanted neural stem cells did not benefit ALS mice by replacing deteriorating nerve cells. Instead, neural stem cells help by producing factors that preserve the health and function of the host’s remaining nerve cells. They also reduce inflammation and suppress the number of disease-causing cells in the host’s spinal cord. These findings, published December 19 in Science Translational Medicine, demonstrate the potential neural stem cells hold for treating ALS and other nervous system disorders.

“While not a cure for human ALS, we believe that the careful transplantation of neural stem cells, particularly into areas that can best sustain life—respiratory control centers, for example—may be ready for clinical trials,” Evan Y. Snyder, M.D., Ph.D., director of Sanford-Burnham’s Stem Cell and Regenerative Biology Program and senior author of the study.

Neural stem cells

In this study, researchers at multiple institutions conducted 11 independent studies to test neural stem cell transplantation in a well-established mouse model of ALS. They all found that this cell therapy reduced the symptoms and course of the ALS-like disease. They observed improved motor performance and respiratory function in treated mice. Neural stem cell transplant also slowed the disease’s progression. What’s more, 25 percent of the treated ALS mice in this study survived for one year or more—roughly three to four times longer than untreated mice.

Neural stem cells are the precursors of all brain cells. They can self-renew, making more neural stem cells, and differentiate, becoming nerve cells or other brain cells. These cells can also rescue malfunctioning nerve cells and help preserve and regenerate host brain tissue. But they’ve never before been studied extensively in a good model of adult ALS.

How neural stem cells benefit ALS mice

Transplanted neural stem cells helped the ALS mice, but not for the obvious reason—not because they became nerve cells, replacing those missing in the ALS spinal cord. The biggest impact actually came from a series of other beneficial neural stem cell activities. It turns out neural stem cells produce protective molecules. They also trigger host cells to produce their own protective molecules. In turn, these factors help spare host nerve cells from further destruction.

Then a number of other positive events take place in treated mice. The transplanted normal neural stem cells change the fate of the host’s own diseased neural stem cells—for the better. This change decreases the number of toxin-producing, disease-promoting cells in the host’s spinal cord. Transplanted neural stem cells also reduce inflammation.

“We discovered that cell replacement plays a surprisingly small role in these impressive clinical benefits. Rather, the stem cells change the host environment for the better and protect the endangered nerve cells,” said Snyder. “This realization is important because most diseases are now being recognized as multifaceted in their cause and their symptoms—they don’t involve just one cell type or one malfunctioning process. We are coming to recognize that the multifaceted actions of the stem cell may address a number of these disease processes.”

Filed under stem cells stem cell transplantation ALS nervous system nerve cells science

2,788 notes

Scientists develop scientific technique to help prevent inherited disorders in humans
A joint team of scientists from The New York Stem Cell Foundation (NYSCF) Laboratory and Columbia University Medical Center (CUMC) has developed a technique that may prevent the inheritance of mitochondrial diseases in children. The study is published online today in Nature.
Dieter Egli, PhD, and Daniel Paull, PhD, of the NYSCF Laboratory with Mark Sauer, MD, and Michio Hirano, MD, of CUMC demonstrated how the nucleus of a cell can be successfully transferred between human egg cells. This landmark achievement carries significant implications for those children who have the potential to inherit mitochondrial diseases.
Mitochondria are cellular organelles responsible for the maintenance and growth of a cell. They contain their own set of genes, passed from mother to child, and are inherited independently from the cell’s nucleus. Although mitochondrial DNA accounts for only 37 out of more than 20,000 genes in an individual, mutations to mitochondrial genes carry harmful effects.
Mitochondrial disorders, due to mutations in mitochondrial DNA, affect approximately 1 in 10,000 people, while nearly 1 in 200 individuals carries mutant mitochondrial DNA. Symptoms, manifesting most often in childhood, may lead to stunted growth, kidney disease, muscle weakness, neurological disorders, loss of vision and hearing, and respiratory problems, among others. Worldwide, a child is born with a mitochondrial disease approximately every 30 minutes, and there are currently no cures for these devastating diseases.
"Through this study, we have shown that it should be possible to prevent the inheritance of mitochondrial disorders," said Egli, PhD, co-author of the study and an Senior Researcher in the NYSCF Laboratory. "We hope that this technique can be advanced quickly toward the clinic where studies in humans can show how the use of this process could help to prevent mitochondrial disease."

Scientists develop scientific technique to help prevent inherited disorders in humans

A joint team of scientists from The New York Stem Cell Foundation (NYSCF) Laboratory and Columbia University Medical Center (CUMC) has developed a technique that may prevent the inheritance of mitochondrial diseases in children. The study is published online today in Nature.

Dieter Egli, PhD, and Daniel Paull, PhD, of the NYSCF Laboratory with Mark Sauer, MD, and Michio Hirano, MD, of CUMC demonstrated how the nucleus of a cell can be successfully transferred between human egg cells. This landmark achievement carries significant implications for those children who have the potential to inherit mitochondrial diseases.

Mitochondria are cellular organelles responsible for the maintenance and growth of a cell. They contain their own set of genes, passed from mother to child, and are inherited independently from the cell’s nucleus. Although mitochondrial DNA accounts for only 37 out of more than 20,000 genes in an individual, mutations to mitochondrial genes carry harmful effects.

Mitochondrial disorders, due to mutations in mitochondrial DNA, affect approximately 1 in 10,000 people, while nearly 1 in 200 individuals carries mutant mitochondrial DNA. Symptoms, manifesting most often in childhood, may lead to stunted growth, kidney disease, muscle weakness, neurological disorders, loss of vision and hearing, and respiratory problems, among others. Worldwide, a child is born with a mitochondrial disease approximately every 30 minutes, and there are currently no cures for these devastating diseases.

"Through this study, we have shown that it should be possible to prevent the inheritance of mitochondrial disorders," said Egli, PhD, co-author of the study and an Senior Researcher in the NYSCF Laboratory. "We hope that this technique can be advanced quickly toward the clinic where studies in humans can show how the use of this process could help to prevent mitochondrial disease."

Filed under mitochondrial diseases cells mutations mitochondrial DNA science

96 notes

How the mind can map negative spaces around the body

The brain’s perception of space can determine whether a part of a body which occupies that space is either healthy or “neglected”.

image

Lorimer Moseley, Chair in Physiotherapy and Professor of Clinical Neurosciences at the University of South Australia, describes recent outcomes of research into spatial perception of people with complex regional pain syndrome (CRPS) as “profound”.

CRPS is a disorder that can develop after a minor injury occurs to a limb and results in abnormal or severe pain developing out of proportion to the nature of the injury. Other problems also result, for example blood flow problems in which the painful arm or leg goes cold and blue, grows too much hair and stays swollen.

In a series of experiments using thermal imaging cameras, changes in the temperature of the hands of people with CRPS were recorded as they moved them across their body midline.

When only the affected hand was crossed over the midline, it became warmer and when only the healthy hand was crossed over the midline, it became cooler.

The temperature change of either hand was positively related to its distance from the body midline and crossing the affected hand over the body midline had small but significant effects on both spontaneous pain (which was reduced) and the sense of ownership over the hand (which was increased).

Professor Moseley said the results of this research indicated that CRPS involves more complex neurological dysfunction than has previously been considered.

“We conclude that impaired spatial perception modulated temperature of the limbs, tactile processing, spontaneous pain and the sense of ownership over the hands.

“This means that the problem that is occurring with the limb relates to the brain process that maps something into a space. It’s almost as though the brain has rejected the space which the limb inhabits.

"In strokes it’s called spatial neglect. This problem with space affects the way blood is sent to the body. If you remove the hand or limb away from that side of space it warms up.

“When you put a healthy hand into the negative space it cools down; the map of space is influencing the rules by which blood flows. Our current finding is clear evidence of the autonomic nervous system being influenced by the brain’s map of space.

“The space itself has adopted the signature of the disorder. This is a profound discovery, it’s a clear physiological phenomena.

“This midline effect changes how much the patient feels the arm belongs to them and how much it hurts.”

(Source: unisa.edu.au)

Filed under regional pain syndrome spatial perception brain pain spatial neglect neuroscience science

585 notes

Study reveals how the brain categorizes thousands of objects and actions
Humans perceive numerous categories of objects and actions, but where are these categories represented spatially in the brain?
Researchers reporting in the December 20 issue of the Cell Press journal Neuron present their study that undertook the remarkable task of determining how the brain maps over a thousand object and action categories when subjects watched natural movie clips. The results demonstrate that the brain efficiently represents the diversity of categories in a compact space. Instead of having a distinct brain area devoted to each category, as previous work had identified, for some but not all types of stimuli, the researchers uncovered that brain activity is organized by the relationship between categories.
"Humans can recognize thousands of categories. Given the limited size of the human brain, it seems unreasonable to expect that every category is represented in a distinct brain area," says first author Alex Huth, a graduate student working in Dr. Jack Gallant’s laboratory at the University of California, Berkeley. The authors proposed that perhaps a more efficient way for the brain to represent object and action categories would be to organize them into a continuous space that reflects the similarity between categories.
To test this hypothesis, they used blood oxygen level-dependent functional magnetic resonance imaging (BOLD fMRI) to measure human brain activity evoked by natural movies in five people. They then mapped out how 1,705 distinct object and action categories are represented across the surface of the cortex of the brain. Their results show that categories are organized as smooth gradients that cover much of the surface of the visual as well as nonvisual cortex, such that similar categories are located next to each other, and notably, this organization was shared across the individuals imaged.
"Discovering the feature space that the brain uses to represent information helps us to recover functional maps across the cortical surface. The brain probably uses similar mechanisms to map other kinds of information across the cortical surface, so our approach should be widely applicable to other areas of cognitive neuroscience," says Dr. Gallant.

Study reveals how the brain categorizes thousands of objects and actions

Humans perceive numerous categories of objects and actions, but where are these categories represented spatially in the brain?

Researchers reporting in the December 20 issue of the Cell Press journal Neuron present their study that undertook the remarkable task of determining how the brain maps over a thousand object and action categories when subjects watched natural movie clips. The results demonstrate that the brain efficiently represents the diversity of categories in a compact space. Instead of having a distinct brain area devoted to each category, as previous work had identified, for some but not all types of stimuli, the researchers uncovered that brain activity is organized by the relationship between categories.

"Humans can recognize thousands of categories. Given the limited size of the human brain, it seems unreasonable to expect that every category is represented in a distinct brain area," says first author Alex Huth, a graduate student working in Dr. Jack Gallant’s laboratory at the University of California, Berkeley. The authors proposed that perhaps a more efficient way for the brain to represent object and action categories would be to organize them into a continuous space that reflects the similarity between categories.

To test this hypothesis, they used blood oxygen level-dependent functional magnetic resonance imaging (BOLD fMRI) to measure human brain activity evoked by natural movies in five people. They then mapped out how 1,705 distinct object and action categories are represented across the surface of the cortex of the brain. Their results show that categories are organized as smooth gradients that cover much of the surface of the visual as well as nonvisual cortex, such that similar categories are located next to each other, and notably, this organization was shared across the individuals imaged.

"Discovering the feature space that the brain uses to represent information helps us to recover functional maps across the cortical surface. The brain probably uses similar mechanisms to map other kinds of information across the cortical surface, so our approach should be widely applicable to other areas of cognitive neuroscience," says Dr. Gallant.

Filed under brain neuron spatial representation brain activity BOLD fMRI neuroscience science

42 notes

Why Our Backs Can’t Read Braille: Scientists map sensory nerves in mouse skin
Johns Hopkins scientists have created stunning images of the branching patterns of individual sensory nerve cells. Their report, published online in the journal eLife on Dec. 18, details the arrangement of these branches in skin from the backs of mice. The branching patterns define ten distinct groups that, the researchers say, likely correspond to differences in what the nerves do and could hold clues for pain management and other areas of neurological study.
Each type of nerve cell that the team studied was connected at one end to the spinal cord through a thin, wire-like projection called an axon. On the other side of the cell’s “body” was another axon that led to the skin. The axons branched in specific patterns, depending on the cell type, to reach their targets within the skin. “The complexity and precision of these branching patterns is breath-taking,” says Jeremy Nathans, M.D., Ph.D., a Howard Hughes researcher and professor of molecular biology and genetics at the Institute for Basic Biomedical Sciences at the Johns Hopkins School of Medicine.
Read more

Why Our Backs Can’t Read Braille: Scientists map sensory nerves in mouse skin

Johns Hopkins scientists have created stunning images of the branching patterns of individual sensory nerve cells. Their report, published online in the journal eLife on Dec. 18, details the arrangement of these branches in skin from the backs of mice. The branching patterns define ten distinct groups that, the researchers say, likely correspond to differences in what the nerves do and could hold clues for pain management and other areas of neurological study.

Each type of nerve cell that the team studied was connected at one end to the spinal cord through a thin, wire-like projection called an axon. On the other side of the cell’s “body” was another axon that led to the skin. The axons branched in specific patterns, depending on the cell type, to reach their targets within the skin. “The complexity and precision of these branching patterns is breath-taking,” says Jeremy Nathans, M.D., Ph.D., a Howard Hughes researcher and professor of molecular biology and genetics at the Institute for Basic Biomedical Sciences at the Johns Hopkins School of Medicine.

Read more

Filed under nerve cells sensory nerve cells skin pain management branching patterns neuroscience science

104 notes

Brake on nerve cell activity after seizures discovered
Given that epilepsy impacts more than 2 million Americans, there is a pressing need for new therapies to prevent this disabling neurological disorder. New findings from the neuroscience laboratory of Mark S. Shapiro, Ph.D., at The University of Texas Health Science Center at San Antonio, published Dec. 20 in the high-impact scientific journal, Neuron, may provide hope.
“A large fraction of epilepsy sufferers cannot take drugs for their disorder or the existing drugs do not manage it,” said Dr. Shapiro, professor of physiology in the School of Medicine. “As a result, many opt for surgery to remove the hippocampus, a part of the brain where memories are stored but also where seizures are often localized. The heart-wrenching choice is between their memories and the epilepsy.”
Genes go into actionA major finding of the study is that selected genes get switched on during and after a seizure, sending swarms of signals to reduce uncontrolled firing of nerve cells. A medication that amplifies this response after a person’s initial seizure could thus prevent recurrent seizures and the onset of devastating epilepsy.
Uncontrolled electrical activity by specialized electricity-producing proteins in the brain called “ion channels” triggers epileptic seizures. One in 10 people have a lifetime risk of suffering a seizure, which can occur for a variety of reasons including traumatic brain injury, stroke or drug overdoses.
A powerful brakeAlthough not all seizures lead to epilepsy, some trigger changes in the brain that heighten the risk of the disorder. Dr. Shapiro’s research sheds light on why most isolated seizures do not lead to full-blown epilepsy, whereas others do. An ion channel called the “M-channel” acts as a powerful “brake” on hyper-excitability in the brain. Another organizational protein, called AKAP79, acting much like an air-traffic controller, calls in more M channels as part of neuroprotective response machinery.
Pharmacological therapy to enhance M-channel gene expression or AKAP79 function “could jump-start this neuroprotective mechanism to prevent a seizure from turning into epilepsy,” Dr. Shapiro said. “Administering it right after a traumatic brain injury could be very effective.”
It was not known that electrical activity could regulate M-channel genes, Dr. Shapiro said. Nor was it known that the AKAP79 organizer protein, which coordinates many aspects of M-channel function, could turn on their genes in a person’s DNA. By increasing M-channel expression in the brain, uncontrolled electrical firing of nerve cells in the brain is sharply controlled.
Mouse experimentsThe Shapiro lab team records electrical currents and performs imaging in living nerve cells to measure M-channel activity. This study included inducing seizures in healthy mice. After a seizure, gene expression of M-channels in the hippocampus increased more than 10-fold within 24 hours, Dr. Shapiro said. This protective effect was completely absent in mice lacking the mouse version of the AKAP79 gene.
“Because excessive firing of nerve cells is also involved in chronic pains, such as migraines, mood disorders and hypertension, increasing M-channel signals to reduce nerve-cell firing could also likely be effective in treating those conditions,” Dr. Shapiro said.

Brake on nerve cell activity after seizures discovered

Given that epilepsy impacts more than 2 million Americans, there is a pressing need for new therapies to prevent this disabling neurological disorder. New findings from the neuroscience laboratory of Mark S. Shapiro, Ph.D., at The University of Texas Health Science Center at San Antonio, published Dec. 20 in the high-impact scientific journal, Neuron, may provide hope.

“A large fraction of epilepsy sufferers cannot take drugs for their disorder or the existing drugs do not manage it,” said Dr. Shapiro, professor of physiology in the School of Medicine. “As a result, many opt for surgery to remove the hippocampus, a part of the brain where memories are stored but also where seizures are often localized. The heart-wrenching choice is between their memories and the epilepsy.”

Genes go into action
A major finding of the study is that selected genes get switched on during and after a seizure, sending swarms of signals to reduce uncontrolled firing of nerve cells. A medication that amplifies this response after a person’s initial seizure could thus prevent recurrent seizures and the onset of devastating epilepsy.

Uncontrolled electrical activity by specialized electricity-producing proteins in the brain called “ion channels” triggers epileptic seizures. One in 10 people have a lifetime risk of suffering a seizure, which can occur for a variety of reasons including traumatic brain injury, stroke or drug overdoses.

A powerful brake
Although not all seizures lead to epilepsy, some trigger changes in the brain that heighten the risk of the disorder. Dr. Shapiro’s research sheds light on why most isolated seizures do not lead to full-blown epilepsy, whereas others do. An ion channel called the “M-channel” acts as a powerful “brake” on hyper-excitability in the brain. Another organizational protein, called AKAP79, acting much like an air-traffic controller, calls in more M channels as part of neuroprotective response machinery.

Pharmacological therapy to enhance M-channel gene expression or AKAP79 function “could jump-start this neuroprotective mechanism to prevent a seizure from turning into epilepsy,” Dr. Shapiro said. “Administering it right after a traumatic brain injury could be very effective.”

It was not known that electrical activity could regulate M-channel genes, Dr. Shapiro said. Nor was it known that the AKAP79 organizer protein, which coordinates many aspects of M-channel function, could turn on their genes in a person’s DNA. By increasing M-channel expression in the brain, uncontrolled electrical firing of nerve cells in the brain is sharply controlled.

Mouse experiments
The Shapiro lab team records electrical currents and performs imaging in living nerve cells to measure M-channel activity. This study included inducing seizures in healthy mice. After a seizure, gene expression of M-channels in the hippocampus increased more than 10-fold within 24 hours, Dr. Shapiro said. This protective effect was completely absent in mice lacking the mouse version of the AKAP79 gene.

“Because excessive firing of nerve cells is also involved in chronic pains, such as migraines, mood disorders and hypertension, increasing M-channel signals to reduce nerve-cell firing could also likely be effective in treating those conditions,” Dr. Shapiro said.

Filed under epileptic seizures epilepsy nerve cells ion channels gene expression neuroscience science

59 notes


Protein Creates Paths For Growing Nerve Cells


Working with mice, Johns Hopkins scientists have discovered that a particular protein helps nerve cells extend themselves along the spinal cord during mammalian development. Their results shed light on the subset of muscular dystrophies that result from mutations in the gene that holds the code for the protein, called dystroglycan, and also show how the nerve and muscle failings of the degenerative diseases are related.


As mammals like mice and humans develop, nerve cells in the brain and spinal cord must form connections with themselves and with muscles to assure proper control of movement. Nerve cells sometimes extend the whole length of the spinal cord to connect sensory nerves bearing information, for example, from the legs to the brain. To do so, nerve cells anchor their “headquarters,” or cell bodies, in one location, and then extend a long, thin projection all the way to their target locations. These projections, or axons, can be 10,000 times longer than the cell body. 


In a report published in the journal Neuron on Dec. 6, the authors suggest that, during fetal development, axons extend themselves along specific pathways created by dystroglycan.

Protein Creates Paths For Growing Nerve Cells

Working with mice, Johns Hopkins scientists have discovered that a particular protein helps nerve cells extend themselves along the spinal cord during mammalian development. Their results shed light on the subset of muscular dystrophies that result from mutations in the gene that holds the code for the protein, called dystroglycan, and also show how the nerve and muscle failings of the degenerative diseases are related.

As mammals like mice and humans develop, nerve cells in the brain and spinal cord must form connections with themselves and with muscles to assure proper control of movement. Nerve cells sometimes extend the whole length of the spinal cord to connect sensory nerves bearing information, for example, from the legs to the brain. To do so, nerve cells anchor their “headquarters,” or cell bodies, in one location, and then extend a long, thin projection all the way to their target locations. These projections, or axons, can be 10,000 times longer than the cell body.

In a report published in the journal Neuron on Dec. 6, the authors suggest that, during fetal development, axons extend themselves along specific pathways created by dystroglycan.

Filed under nerve cells neurodegenerative diseases spinal cord mammalian development protein neuroscience science

67 notes

Helping the nose know: Researcher answers 100-year-old question about how olfactory feedback mechanism works
More than a century after it was first identified, Harvard scientists are shedding new light on a little-understood neural feedback mechanism that may play a key role in how the olfactory system works in the brain.
As described in a December 19 paper in Neuron by Venkatesh Murthy, Professor of Molecular and Cellular Biology, researchers have, for the first time, described how that feedback mechanism works by identifying where the signals go, and which type of neurons receive them. Three scientists from the Murthy lab were involved in the work: Foivos Markopoulos, Dan Rokni and David Gire.
"The image of the brain as a linear processor is a convenient one, but almost all brains, and certainly mammalian brains, do not rely on that kind of pure feed-forward system," Murthy explained. "On the contrary, it now appears that the higher regions of the brain which are responsible for interpreting olfactory information are communicating with lower parts of the brain on a near-constant basis."
Though researchers have known about the feedback system for decades, key questions about its precise workings, such as which neurons in the olfactory bulb receive the feedback signals, remained a mystery, partly because scientists simply didn’t have the technological tools needed to activate individual neurons and individual pathways.
"One of the challenges with this type of research is that these feedback neurons are not the only neurons that come back to the olfactory bulb," Murthy explained. "The challenge has always been that there’s no easy way to pick out just one type of neuron to activate."
To do it, Murthy and his team turned to a technique called optogenetics.
Using a virus that has been genetically-modified to produce a light-sensitive protein, Murthy and his team marked specific neurons, which become active when hit with laser light. Researchers were then able to trace the feedback mechanism from the brain’s processing centers back to the olfactory bulb.
Reaching that level of precision was critical, Murthy explained, because while olfactory bulb contains many “principal” neurons which are responsible for sending signals on to other parts of the brain, it is also packed with interneurons, which appear to play a role in formatting olfactory information as it comes into the brain.
(Image: BigStock)

Helping the nose know: Researcher answers 100-year-old question about how olfactory feedback mechanism works

More than a century after it was first identified, Harvard scientists are shedding new light on a little-understood neural feedback mechanism that may play a key role in how the olfactory system works in the brain.

As described in a December 19 paper in Neuron by Venkatesh Murthy, Professor of Molecular and Cellular Biology, researchers have, for the first time, described how that feedback mechanism works by identifying where the signals go, and which type of neurons receive them. Three scientists from the Murthy lab were involved in the work: Foivos Markopoulos, Dan Rokni and David Gire.

"The image of the brain as a linear processor is a convenient one, but almost all brains, and certainly mammalian brains, do not rely on that kind of pure feed-forward system," Murthy explained. "On the contrary, it now appears that the higher regions of the brain which are responsible for interpreting olfactory information are communicating with lower parts of the brain on a near-constant basis."

Though researchers have known about the feedback system for decades, key questions about its precise workings, such as which neurons in the olfactory bulb receive the feedback signals, remained a mystery, partly because scientists simply didn’t have the technological tools needed to activate individual neurons and individual pathways.

"One of the challenges with this type of research is that these feedback neurons are not the only neurons that come back to the olfactory bulb," Murthy explained. "The challenge has always been that there’s no easy way to pick out just one type of neuron to activate."

To do it, Murthy and his team turned to a technique called optogenetics.

Using a virus that has been genetically-modified to produce a light-sensitive protein, Murthy and his team marked specific neurons, which become active when hit with laser light. Researchers were then able to trace the feedback mechanism from the brain’s processing centers back to the olfactory bulb.

Reaching that level of precision was critical, Murthy explained, because while olfactory bulb contains many “principal” neurons which are responsible for sending signals on to other parts of the brain, it is also packed with interneurons, which appear to play a role in formatting olfactory information as it comes into the brain.

(Image: BigStock)

Filed under olfactory bulb olfactory system neuron cerebral cortex optogenetics neuroscience science

free counters