Posts tagged neuron
Articles and news from the latest research reports.
Purkinje neurons (yellow) generated from embryonic stem cells integrate into the cerebellum (red) when transplanted into the fetal mouse brain.
© 2010 K. Muguruma et al.
New treatments for epilepsy, behavioral disorders could result from Wayne State University studies
Three studies conducted as part of Wayne State University’s Systems Biology of Epilepsy Project (SBEP) could result in new types of treatment for the disease and, as a bonus, for behavioral disorders as well.
The SBEP started out with funds from the President’s Research Enhancement Fund and spanned neurology, neuroscience, genetics and computational biology. It since has been supported by multiple National Institutes of Health-funded grants aimed at identifying the underlying causes of epilepsy, and it is uniquely integrated within the Comprehensive Epilepsy Program at the Wayne State School of Medicine and the Detroit Medical Center.
Under the guidance of Jeffrey Loeb, M.D., Ph.D., associate director of the Center for Molecular Medicine and Genetics (CMMG) and professor of neurology, the project brings together researchers from different fields to create an interdisciplinary research program that targets the complex disease. The multifaceted program at Wayne State is like no other in the world, officials say, with two primary goals: improving clinical care and creating novel strategies for diagnosis and treatment of patients with epilepsy.
(Source: research.wayne.edu)
Study gives clues to causes of Motor Neurone Disease
Scientists at the University of Bath are one step further to understanding the role of one of the proteins that causes the neurodegenerative disorder, Amyotrophic Lateral Sclerosis (ALS), also known as Motor Neurone Disease (MND).
The scientists studied a protein called angiogenin, which is present in the spinal cord and brain that protects neurones from cell death. Mutations in this protein have been found in sufferers of MND and are thought to play a key role in the progression of the condition.
MND triggers progressive weakness, muscle atrophy and muscle twitches and spasms. The disease affects around 5000 people in the UK.
The team of cell biologists and structural biologists have, for the first time, produced images of the 3D structures of 11 mutant versions of angiogenin to see how the mutations changed the structure of the active part of the molecule, damaging its function.
The study, published in the prestigious journal Nature Communications, provides insights into the causes of this disease and related conditions such as Parkinson’s Disease.
The team also looked at the effects of the malfunctioning proteins on neurones grown from embryonic stem cells in the laboratory.
They found that some of the mutations stopped the protein being transported to the cell nucleus, a process that is critical for the protein to function correctly.
The mutations also prevented the cells from producing stress granules, the neurone’s natural defence from stress caused by low oxygen levels.
Dr Vasanta Subramanian, Reader in Biology & Biochemistry at the University, said:
“This study is exciting because it’s the first time we’ve directly linked the structure of these faulty proteins with their effects in the cell.
“We’ve worked alongside Professor Ravi Acharya’s group to combine structural knowledge with cell biology to gain new insights into the causes of this devastating disease.
“We hope that the scientific community can use this new knowledge to help design new drugs that will bind selectively to the defective protein to protect the body from its damaging effects.”
The findings were welcomed by medical research charity, the Motor Neurone Disease (MND) Association, the only national charity in England, Wales and Northern Ireland dedicated to supporting people living with MND while funding and promoting cutting-edge global research to bring about a world free of the disease.
Dr Brian Dickie, Director of Research Development at the charity, said: “The researchers at the University of Bath have skilfully combined aspects of biology, chemistry and physics to answer some fundamental questions on how angiogenin can damage motor neurones. It not only advances our understanding of the disease, but may also give rise to new ideas on treatment development.”
(Source: bath.ac.uk)
Let there be sight: Burst of neural activity necessary for vision
A sudden and mysterious burst of activity originating in the retina of a developing fetus spurs brain connections that are essential to development of finely-tuned sight, Yale researchers report in the journal Nature. Interference with this spontaneous wave of activity could play a role in neurodevelopmental disorders such as autism, the scientists speculate.
The study in mice is the first to demonstrate in a living animal that this wave of activity spreads throughout large regions of the brain and is crucial to wiring of the visual system. Without the wiring, infants would not be able to distinguish details in their environment.
“If you interfere with this activity, the circuits are all messed up, the wiring details are all wrong,” said Michael Crair, the William Ziegler III Professor of Neurobiology and Professor of Ophthalmology and Visual Science and senior author of the study.
For instance, this activity might allow a newborn human baby to perceive such details as the five fingers attached to her hand or her mother’s face. This wave wires up the visual system so that infants are poised to learn from their environment soon after birth.
The development of animals from a fertilized egg into trillions of intricately connected and specialized cells is the result of a precisely timed expression of genes. However, the Nature paper introduces another necessary factor — a mysterious wave of activity arising in the retina itself that propagates through several regions of the brain. Crair terms this wave an emergent property, or a trait possessed by a complex system that cannot be directly traced to its individual parts. This experiment in living, neonatal mice shows that this wave is crucial to the proper wiring not only of the visual system but other brain areas as well.
Crair said his lab plans to explore whether interruptions of this activity might play a role in neurodevelopmental disorders such as autism or schizophrenia.
(Source: news.yale.edu)
What Drives Your Daily Biological Clock?
Researchers working with fruit flies say they have discovered one way that the body’s biological clock controls brain-cell activity that influences daily rhythms.
They believe their findings might improve understanding about sleep-wake cycles and lead to new treatments for sleep disorders and jet lag.
"The findings answer a significant question: how biological clocks drive the activity of clock neurons, which, in turn, regulate behavioral rhythms," study senior author Justin Blau, associate professor in New York University’s department of biology, said in a university news release.
Previous research with fruit flies’ “clock genes” led to the discovery of similar genes in humans, according to the news release.
It was known that biological clocks control neuronal activity, but it wasn’t known how information from biological clocks drives rhythms in the electrical activity of pacemaker neurons that control daily rhythms.
The NYU team looked at pacemaker neurons in the central brain of fruit flies that set the timing of the daily transitions between sleep and wake. They isolated these neurons and identified sets of genes with different levels of activity at dawn and dusk.
Follow-up experiments found that the activity of a gene called Ir was much higher at dusk than at dawn and that it was more active in the pacemaker neurons than in the rest of the brain. The researchers also found that increasing or decreasing levels of Ir affected behavioral rhythms and changed the timing and strength of variations in the core clock.
"We were looking for an output of the biological clock that would link the core clock to neuronal activity," Blau said. "Ir seems to do this, but it also, remarkably, feeds back to regulate the core clock itself. Feedback loops seem to be deeply engrained into the biological clock and presumably help these clocks work so well."
The study was published in the October issue of the Journal of Biological Rhythms. Researchers have noted that results from animal studies do not necessarily translate to humans.
Memory: Do animals ever forget?
From pigeons that can recognise faces to a chimp that stores rocks to throw at visitors, all animals have memories. But how similar are they to ours?
(Image: Matt Jacob/Tendance Floue)
EVERY morning, you take a walk in the park, bringing some bread to feed the pigeons. As the days wear on, you begin to see the birds as individuals; you even start to name them. But what do the pigeons remember of you? Do they think kindly of you as they drop off to sleep at night, or is your face a blank, indistinguishable from the others strolling through the park?
These questions may seem whimsical, but knowing what other creatures recall is crucial if we are to understand their inner lives. It turns out that the range of mnemonic feats in the wild is nearly as varied as life itself.
If you take memory to mean any ability to store and respond to past events, even the simplest organisms meet the grade. Blobs of slime mould, for instance, which can slowly crawl across a surface, seem to note the timing of changes to their climate, slowing their movement in anticipation of an expected dry spell - even when it never actually arrives.
With the emergence of the first neurons about half a billion years ago, memories became more intricate as information could be stored in the patterns of electrical connections within the nervous system. This type of learning may have been behind the Cambrian explosion - the sudden appearance and rapid evolution of more complex species about 530 million years ago - because it enabled animals to exploit new niches, say Eva Jablonka at Tel Aviv University and Simona Ginsburg at the Open University of Israel.
Over the following few hundred million years, increasingly advanced skills could emerge with different forces driving the evolution of each creature’s mind. The result is a surprising range of mnemonic feats throughout the animal kingdom. Migratory cardinal fish, for instance, can remember where they laid their eggs during the breeding season and, after over-wintering in deep water, return to within half a metre of the same spot. Animals as diverse as lizards, bees and octopuses can learn the way out of a maze, and pigeons have an excellent visual recognition, learning to recognise more than a thousand different images. They can even recognise individual humans and aren’t fooled by a change of clothes.
Such skills, although impressive, don’t match our experiences of episodic memory, in which we immerse ourselves in specific events. A pigeon might learn to associate your face with food, but it probably can’t remember your last meeting in the way you might be able to recall details of your last trip to the park.
Dual spotlights in the brain
How we manage to attend to multiple objects without being distracted by irrelevant information
The “tiki-taka”-style of the Spanish national football team is amazing to watch: Xavi passes to Andrès Iniesta, he just rebounds the ball once and it’s right at Xabi Alonso’s foot. The Spanish midfielders cross the field as if they run on rails, always maintaining attention on the ball and the teammates, the opponents chasing after them without a chance. An international team of scientists from the German Primate Center and McGill University in Canada, including Stefan Treue, head of the Cognitive Neuroscience Laboratory, has now uncovered how the human brain makes such excellence possible by dividing visual attention: The brain is capable of splitting its ‘attentional spotlight’ for an enhanced processing of multiple visual objects. (Neuron, doi: 10.1016/j.neuron.2011.10.013)
When we pay attention to an object, neurons responsible for this location in our field of view are more active then when they process unattended objects. But quite often we want to pay attention to multiple objects in different spatial positions, with interspersed irrelevant objects. Different theories have been proposed to account for this ability. One is, that the attentive focus is split spatially, excluding objects between the attentional spotlights. Another possibility is, that the attentional focus is zoomed out to cover all relevant objects, but including the interspersed irrelevant ones. A third possibility would be a single focus rapidly switching between the attended objects.
Studying rhesus macaques
In order to explain how such a complex ability is achieved, the neuroscientists measured the activity of individual neurons in areas of the brain involved in vision. They studied two rhesus macaques, which were trained in a visual attention task. The monkeys had learned to pay attention to two relevant objects on a screen, with an irrelevant object between them. The experiment showed, that the macaques’ neurons responded strongly to the two attended objects with only a weak response to the irrelevant stimulus in the middle. So the brain is able to spatially split visual attention and ignore the areas in between. “Our results show the enormous adaptiveness of the brain, which enables us to deal effectively with many different situations.
This multi-tasking allows us to simultaneously attend multiple objects”, Stefan Treue says. Such a powerful ability of our attentive system is one precondition for humans to become perfect football-artists but also to safely navigate in everyday traffic.
(Source: alphagalileo.org)
Wasp has hints of a clockwork brain
The greenhouse whitefly parasite (Encarsia formosa) is just half a millimetre in length. It parasitises the larvae of whiteflies and so it has long been used as a natural pest-controller.
To find out how its neurons have adapted to miniaturisation, Reinhold Hustert of the University of Göttingen in Germany examined the insect’s brain with an electron microscope. The axons - fibres that shuttle messages between neurons - were incredibly thin. Of 528 axons measured, a third were less than 0.1 micrometre in diameter, an order of magnitude narrower than human axons. The smallest were just 0.045 μm (Arthropod Structure & Development, doi.org/jfn).
That’s a surprise, because according to calculations by Simon Laughlin of the University of Cambridge and colleagues, axons thinner than 0.1 μm simply shouldn’t work. Axons carry messages in waves of electrical activity called action potentials, which are generated when a chemical signal causes a large number of channels in a cell’s outer membrane to open and allow positively charged ions into the axon. At any given moment some of those channels may open spontaneously, but the number involved isn’t enough to accidentally trigger an action potential, says Laughlin - unless the axon is very thin. An axon thinner than 0.1 μm will generate an action potential if just one channel opens spontaneously (Current Biology, doi.org/frfwpz).
"That makes the axon impossibly noisy," Laughlin says. Any "legitimate" action potentials will be drowned out.
Hustert suggests that a neuron might get around this problem by firing bursts of action potentials to cut through the noise, but Laughlin is sceptical. “They’d be firing furiously all the time,” he says, and every action potential costs energy.
Instead, the neurons might not bother with conventional action potentials at all. “They could be sending signals mechanically,” Laughlin says. The tiny axons might each carry a long rigid rod stretching down the centre. Pulling the rod could create a physical rather than electrical trigger for the release of a chemical that passes the signal on to the neighbouring neuron.
In larger animals this would be far too slow, says Laughlin, but in the tiny body of the greenhouse whitefly parasite, a partly “clockwork” brain might be the best approach.
Morphine and cocaine affect reward sensation differently
A new study by scientists in the US has found that the opiate morphine and the stimulant cocaine act on the reward centers in the brain in different ways, contradicting previous theories that these types of drugs acted in the same way.
Morphine and cocaine both affect the flow of the neurotransmitter dopamine, which has been shown to be important in the feeling of reward. When a dopamine neuron is stimulated it releases dopamine, which is then taken up by neighboring cells. Any excess is reabsorbed into the original dopamine neuron by a process known as “reuptake.”
Cocaine is known to block reuptake, and the excess dopamine leads to an enhanced reward effect. Cocaine is also known to make the cells in the nucleus accumbens, which receives signals from the VTA, more sensitive to cocaine. It was already known a protein called brain-derived neurotrophic factor (BDNF) in the VTA region of the brain enhances the reward response to cocaine.
The new study shows that BDNF has the opposite effect when morphine is present, decreasing the reward response and the development of addiction rather than enhancing it. The researchers identified numerous genes regulated by BDNF and associated with its effects. They used genetic techniques to suppress BDNF, and then directly excited the neurons in the nucleus accumbens that normally receives transmitted impulses from the VTA.
They found that suppressing BDNF in the VTA allowed morphine to increase the excitability of dopamine neurons and hence enhance the reward. When they optically excited the dopamine terminals in the nucleus accumbens that normally receive the transmissions from the VTA, they also found a reversal in the normal effect of BDNF.