ScienceDaily (May 25, 2012) — UC Davis mathematicians have helped biologists figure out why platelets, the cells that form blood clots, are the size and shape that they are. Because platelets are important both for healing wounds and in strokes and other conditions, a better understanding of how they form and behave could have wide implications.

"Platelet size has to be very specific for blood clotting," said Alex Mogilner, professor of mathematics, and neurobiology, physiology and behavior at UC Davis and a co-author of the paper, published this week in the journal Nature Communications. “It’s a longstanding puzzle in platelet formation, and this is the first quantitative solution.”

Mogilner and UC Davis postdoctoral scholars Jie Zhu and Kun-Chun Lee developed a mathematical model of the forces inside the cells that turn into platelets, accurately predicting their final size and shape.

They were collaborating with a team led by Joseph Italiano and Jonathon Thon at Harvard Medical School and Brigham and Women’s Hospital, Boston.

Platelets are made by bone marrow cells called megakaryocytes. They bud off first as large, circular pre-platelets, form into a dumbbell-shaped pro-platelet, then finally divide into a standard-sized, disc-shaped platelet. A typical person has about a trillion platelets in circulation at a time, and makes about 100 billion new platelets a day, each living for 8 to 10 days.

Inside the pre- and pro-platelets is a ring of protein microtubules, which exerts pressure to straighten and broaden the nascent cells. But overlying the ring is a rigid cortex of proteins that prevents the platelets from expanding.

By tweaking the number of microtubules in the bundles, Mogilner, Zhu and Lee found that they could correctly predict how pro-platelets would flip into a dumbbell shape, as well as the size and shape of mature platelets.

Source: Science Daily

May 25, 2012 by Stuart Mason Dambrot

(Medical Xpress) — Regardless of an organism’s biological complexity, every encephalized animal continuously makes under-informed behavioral choices that can have serious consequences. Despite its ubiquity, however, there’s a long-standing question about its neurological basis – namely, whether these choices are made through probabilistic world models constructed by the brain, or by reinforcement of learned associations. Recently, however, scientists in the Department of Psychology at Rutgers University found that reinforcement cannot account for the rapidity with which mice modify their behavior when the chance of a given phenomenon changes. The researchers say this indicates that mice may have primordially-evolved neural capabilities to represent likelihood and perform calculations that optimize their resulting behavior – and therefore that such genetic mechanisms can be investigated and manipulated by genetic and other procedures.

The experimental environment. In the switch task, a trial proceeds as follows: 1: Light in the Trial-Initiation Hopper signals that the mouse may initiate a trial. 2: The mouse approaches and pokes into the trial-initiation hopper, extinguishing the light there and turning on the lights in the two feeding hoppers (trial onset). 3: The mouse goes to the short-latency hopper and pokes into it. 4: If, after 3 s have elapsed since the trial onset, poking in the short-latency hopper does not deliver a pellet, the mouse switches to the long-latency hopper, where it gets a pellet there in response to the first poke at or after 9 s since the trial onset. Lights in both feeding hoppers extinguish either at pellet delivery or when an erroneously timed poke occurs. Short trials last about 3 s and long trials about 9 s, whether reinforced or not: if the mouse is poking in the short hopper at the end of a 3-s trial, it gets a pellet and the trial ends; if it is poking in the 9-s hopper, it does not get a pellet and the trial ends at 3 s. Similarly, long trials end at 9 s: if the mouse is poking in the 9-s hopper, it gets a pellet; if in the 3-s hopper, it does not. A switch latency is the latency of the last poke in the short hopper before the mouse switches to the long hopper. Only the switch latencies from long trials are analyzed. Copyright © PNAS, doi: 10.1073/pnas.1205131109

In conducting their research, Prof. Randy Gallistel and doctoral student Aaron Kheifets had to first address a key challenge in identifying estimates of stochastic parameters versus reinforcement-driven processes as the behavior-optimizing mechanism in the laboratory mice studied (the c57bl/6j strain of Mus musculus, the common house mouse, from Jackson Labs). “Because both processes can lead to approximately optimal behavior in the long run,” Gallistel tells Medical Xpress, “one has to focus on the short run – that is, on the course of the transition in behavior. The problem in this case is that the transition is a change in the distribution of switch latencies.” A distribution of switch latencies is composed of a great many temporal discriminations on the part of the subject observed over a long sequence of trials, so this distribution can be used to prove that the process generating the distribution changed abruptly.

“Fortunately,” Gallistel continues, “it was obvious from simple inspection of the raw data that there was an abrupt change. The challenge was to develop a mathematical analysis that confirmed this. Meeting this challenge required the use of Bayesian methods, which are just now beginning to be applied to behavioral data. In addition, we had to develop analyses showing that differential reinforcement could not explain the transition.” The team therefore applied Bayesian methods of analysis to the determination of the parameters of a transition function for a 4-parameter mixture distribution.

“Also,” Gallistel adds, “a graphical means of displaying the raw data in such a way as to make the basic phenomenon visually apparent was required. To this end, we devised a figure with a huge number of bits per square centimeter – that is, it shows an enormous amount of readily graspable information in a small space.”

Read more …

ScienceDaily (May 24, 2012) — Experiencing strong emotions synchronizes brain activity across individuals, a research team at Aalto University and Turku PET Centre in Finland has revealed.

Experiencing strong emotions synchronizes brain activity across individuals. (Credit: Image courtesy of Aalto University)

Human emotions are highly contagious. Seeing others’ emotional expressions such as smiles triggers often the corresponding emotional response in the observer. Such synchronization of emotional states across individuals may support social interaction: When all group members share a common emotional state, their brains and bodies process the environment in a similar fashion.

Researchers at Aalto University and Turku PET Centre have now found that feeling strong emotions makes different individuals’ brain activity literally synchronous.

The results revealed that especially feeling strong unpleasant emotions synchronized brain’s emotion processing networks in the frontal and midline regions. On the contrary, experiencing highly arousing events synchronized activity in the networks supporting vision, attention and sense of touch.

"Sharing others’ emotional states provides the observers a somatosensory and neural framework that facilitates understanding others’ intentions and actions and allows to ‘tune in’ or ‘sync’ with them. Such automatic tuning facilitates social interaction and group processes," says Adjunct Professor Lauri Nummenmaa from the Aalto University, Finland.

"The results have major implications for current neural models of human emotions and group behavior. It also deepens our understanding of mental disorders involving abnormal socioemotional processing," Nummenmaa says.

Participants’ brain activity was measured with functional magnetic resonance imaging while they were viewing short pleasant, neutral and unpleasant movies.

Source: Science Daily

ScienceDaily (May 24, 2012) — Researchers have identified a protein necessary to maintain behavioral flexibility, which allows us to modify our behaviors to adjust to circumstances that are similar, but not identical, to previous experiences. Their findings, which appear in the journal Cell Reports, may offer new insights into addressing autism and schizophrenia — afflictions marked by impaired behavioral flexibility.

Our stored memories from previous experiences allow us to repeat certain tasks. For instance, after driving to a particular location, we recall the route the next time we make that trip. However, sometimes circumstances change — one road on the route is temporarily closed — and we need to make adjustments to reach our destination. Our behavioral flexibility allows us to make such changes and, then, successfully complete our task. It is driven, in part, by protein synthesis, which produces experience-dependent changes in neural function and behavior.

However, this process is impaired for many, preventing an adjustment in behavior when faced with different circumstances. In the Cell Reports study, the researchers sought to understand how protein synthesis is regulated during behavioral flexibility.

To do so, they focused on the kinase PERK, an enzyme that regulates protein synthesis. PERK is known to modify eIF2α, a factor that is required for proper protein synthesis. Their experiments involved comparing normal lab mice, which possessed the enzyme, with those that lacked it.

In their study, the mice were asked to navigate a water maze, which included elevating themselves onto a platform to get out of the water. Normal mice and those lacking PERK learned to complete this task.

However, in a second step, the researchers tested the mice’s behavioral flexibility by moving the maze’s platform to another location, thereby requiring them to respond to a change in the terrain. Here, the normal mice located the platform, but those lacking PERK were unable to do so or took significantly more time to complete the task.

A second experiment offered a different test of the role of PERK in aiding behavioral flexibility. In this measure, both normal and mutant mice heard an audible tone that was followed by a mild foot shock. At this stage, all of the mice developed a normal fear response — freezing at the tone in anticipation of the foot shock. However, the researchers subsequently removed the foot shock from the procedure and the mice heard only the tone. Eventually, the normal mice adjusted their responses so they did not freeze after hearing the tone. However, the mutant mice continued to respond as if they expected a foot shock to follow.

The researchers sought additional support for their conclusion that the absence of PERK may contribute to impaired behavioral flexibility in human neurological disorders. To do so, they conducted postmortem analyses of human frontal cortex samples from patients afflicted with schizophrenia, who often exhibit behavioral inflexibility, and unaffected individuals. The samples from the control group showed normal levels of PERK while those from the schizophrenic patients had significantly reduced levels of the protein.

"A rapidly expanding list of neurological disorders and neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and Fragile X syndrome, have already been linked to aberrant protein synthesis," explained Eric Klann, a professor in NYU’s Center for Neural Science and one of the study’s co-authors. "Our results show the significance of PERK in maintaining behavioral flexibility and how its absence might be associated with schizophrenia. Further studies clarifying the specific role of PERK-regulated protein synthesis in the brain may provide new avenues to tackle such widespread and often debilitating neurological disorders."

Source: Science Daily

May 24, 2012

A molecule responsible for the proper formation of a key portion of the nervous system finds its way to the proper place not because it is actively recruited, but instead because it can’t go anywhere else.

Researchers at Baylor College of Medicine have identified a distal axonal cytoskeleton as the boundary that makes sure AnkyrinG clusters where it needs to so it can perform properly.

The findings appear in the current edition of Cell.

"It has been known that AnkyrinG is needed for the axon initial segment to form. Without the axon initial segment there would be no output of information within the nervous system,” said Dr. Matthew Rasband, associate professor of neuroscience at BCM. “Every known protein found at the axon initial segment depends on AnkyrinG, so if it is eliminated then the axon initial segment doesn’t form and the neuron doesn’t fire.”

To answer the question of how AnkyrinG gets to where it needs to be for proper function, Rasband, along with first author Dr. Mauricio Galiano, postdoctoral associate in neuroscience at BCM, and colleagues, began by analyzing how the axon initial segment forms. They found that AnkyrinG always appeared in exactly the same spot during development.

"It would start to enter into the axon and then it was almost as if it hit a wall and couldn’t go any further," Rasband said. "We would see it stop very close to the cell body and then it would backfill. This showed us that there was some type of boundary or barrier marking that area."

To further study the properties of the boundary they began to look at ways they could disrupt or move it to test the effects of AnkyrinG clustering in different areas.

In cell cultures mouse models they were able to move the boundary to different distances along the axon. Doing this allowed researchers to change the length of the axon initial segment. If the boundary was farther away from the cell body than the length of the segment was longer. If it was closer to the cell body, then the length was shorter.

When researchers removed the boundary all together, AnkyrinG would not cluster in the appropriate area and the axon initial segment would not form.

"We had anticipated there was a kind of molecule that recruited AnkyrinG but instead we found a barrier that excludes it," Rasband said. "These results have important implications because they imply a similar exclusion mechanism might be in play or functioning not only at the axon initial segment, but all of the places where AnkyrinG is found."

Rasband said within many disorders like autism or epilepsy proteins that AnkyrinG is responsible for forming are disrupted. So understanding how this molecule functions properly could one day play a role in finding treatment targets for diseases.

Provided by Baylor College of Medicine

Source: medicalxpress.com

May 24, 2012

Like emergency workers rushing to a disaster scene, cells called microglia speed to places where the brain has been injured, to contain the damage by ‘eating up’ any cellular debris and dead or dying neurons. Scientists at the European Molecular Biology Laboratory (EMBL) in Heidelberg, Germany, have now discovered exactly how microglia detect the site of injury, thanks to a relay of molecular signals. Their work, published today in Developmental Cell, paves the way for new medical approaches to conditions where microglia’s ability to locate hazardous cells and material within the brain is compromised.

Microglia (green) move to the site of injury (arrow) to clear up debris. Credit: Copyright EMBL/Peri

"Considering that they help keep our brain healthy, we know surprisingly little about microglia," says Francesca Peri, who led the work. "Now, for the first time, we’ve identified the mechanism that allows microglia to detect brain injury, and how that emergency call is transmitted from neuron to neuron.”

When microglia (green) cannot detect ATP (bottom), they don’t move to the injury site as they usually would (top). Credit: Copyright EMBL/Peri

When an emergency occurs, cries can alert bystanders, who will dial the emergency number. A call will go out over the radio, and ambulances, police or fire engines in the area will respond as needed. In the brain, Peri and colleagues found, injured neurons send out their own distress cry: they release a molecule called glutamate. Neighbouring neurons sense that glutamate and respond by taking up calcium. As glutamate spreads out from the injury site, this creates a wave of calcium swallowing. Along that wave, as neurons take up calcium they release a third molecule, called ATP. When the wave comes within reach, a microglial cell detects that ATP and takes it as a call to action, moving in that direction – essentially tracing the wave backwards until it reaches the injury.

Scientists knew already that microglia can detect ATP, but this molecule doesn’t last long outside of cells, so there were doubts about how ATP alone could be a signal that carried far enough to reach microglia located far from the site of injury. The trick, as Peri and colleagues discovered, is the long-lasting glutamate-driven calcium wave that can travel the length of the brain. Thanks to this wave, the ATP signal is not just emitted by the injured cells, but is repeatedly sent out by the neurons along the way, until it reaches microglia.

Dirk Sieger and Christian Moritz in Peri’s lab took advantage of the fact that zebrafish have transparent heads, which allow scientists to peer down a microscope straight into the fish’s brain. They used a laser to injure a few of the fish’s brain cells, and watched fluorescently-labelled microglia move in on the injury. When they genetically engineered zebrafish to make neurons’ calcium levels traceable under the microscope, too, the scientists were able to confirm that when the calcium wave reached microglia, these cells immediately started moving toward the injury.

Knowing all the steps in this process, and how they feed into each other, could help to design treatments to improve microglia’s detection ability, which go awry in conditions such as Alzheimer’s and Parkinson’s diseases.

Provided by European Molecular Biology Laboratory

Source: medicalxpress.com

May 24, 2012

Despite a long-held scientific belief that much of the wiring of the brain is fixed by the time of adolescence, a new study shows that changes in sensory experience can cause massive rewiring of the brain, even as one ages. In addition, the study found that this rewiring involves fibers that supply the primary input to the cerebral cortex, the part of the brain that is responsible for sensory perception, motor control and cognition. These findings promise to open new avenues of research on brain remodeling and aging.

Published in the May 24, 2012 issue of Neuron, the study was conducted by researchers at the Max Planck Florida Institute (MPFI) and at Columbia University in New York.

"This study overturns decades-old beliefs that most of the brain is hard-wired before a critical period that ends when one is a young adult," said MPFI neuroscientist Marcel Oberlaender, PhD, first author on the paper. "By changing the nature of sensory experience, we were able to demonstrate that the brain can rewire, even at an advanced age. This may suggest that if one stops learning and experiencing new things as one ages, a substantial amount of connections within the brain may be lost."

The researchers conducted their study by examining the brains of older rats, focusing on an area of the brain known as the thalamus, which processes and delivers information obtained from sensory organs to the cerebral cortex. Connections between the thalamus and the cortex have been thought to stop changing by early adulthood, but this was not found to be the case in the rodents studied.

Being nocturnal animals, rats mainly rely on their whiskers as active sensory organs to explore and navigate their environment. For this reason, the whisker system is an ideal model for studying whether the brain can be remodeled by changing sensory experience. By simply trimming the whiskers, and preventing the rats from receiving this important and frequent form of sensory input, the scientists sought to determine whether extensive rewiring of the connections between the thalamus and cortex would occur.

On examination, they found that the animals with trimmed whiskers had altered axons, nerve fibers along which information is conveyed from one neuron (nerve cell) to many others; those whose whiskers were not trimmed had no axonal changes. Their findings were particularly striking as the rats were considered relatively old – meaning that this rewiring can still take place at an age not previously thought possible. Also notable was that the rewiring happened rapidly – in as little as a few days.

"We’ve shown that the structure of the rodent brain is in constant flux, and that this rewiring is shaped by sensory experience and interaction with the environment," said Dr. Oberlaender. "These changes seem to be life-long and may pertain to other sensory systems and species, including people. Our findings open the possibility of new avenues of research on development of the aging brain using quantitative anatomical studies combined with noninvasive imaging technologies suitable for humans, such as functional MRI (fMRI)."

The study was possible due to recent advances in high-resolution imaging and reconstruction techniques, developed in part by Dr. Oberlaender at MPFI. These novel methods enable researchers to automatically and reliably trace the fine and complex branching patterns of individual axons, with typical diameters less than a thousandth of a millimeter, throughout the entire brain.

Provided by Tartaglia Communications

Source: medicalxpress.com

May 24, 2012

The birth of sensory perception on the human cerebral cortex is yet to be fully explained. The different areas on the cortex function in cooperation, and no perception is the outcome of only one area working alone. In his doctoral dissertation for the Department of Biomedical Engineering and Computational Science in Aalto University Jaakko Kauramäki shows that the auditory cortex is not left to its own devices.

Kauramäki’s dissertation in the field of cognitive neuroscience studied neural top-down processes, that is, the ways the brain as a system handles sounds arriving onto the auditory cortex in the frontal lobes.

Moving from parts towards a whole, bottom-up processes analyse a sound by dissecting it in hierarchical chain reactions from small and sophisticated bits towards a concise auditory sensation.

"The operation of the system as a whole can be affected by focusing on a specific task or sound. In my research I focused precisely on how the top-down effects manifest themselves on the auditory cortex," explains Kauramäki his study.

Right kind of noise promotes concentration and reinforces perception?

Kauramäki studied the auditory cortex in two separate tasks: reactions caused by selective attention during sound recognition and by lipreading. Kauramäki recorded the electrical and magnetic activity on the cortex using electroencephalography (EEG) and magnetoencephalography (MEG) respectively.

"40 years ago a so-called ‘gain effect’ was formulated: focusing attention enhances responses on the auditory cortex, which means that attention helps to better perceive audio stimuli," tells Kauramäki.

In the attention tests Kauramäki masked the sounds played for the test subjects with different frequencies of noise – and made a discovery. During periods of selective attention, the enhanced responses on the auditory cortex depended on the type of noise used. The frequency content of the noise affected the prominence of the responses. The responses are not only enhanced, but they are feature and task-specific.

"Similar results have not been obtained earlier because the stimuli used in the experiments have been too simple. The noise mask added a combinatory effect that brought the specificity and selectivity of the responses to the fore."

"Focusing attention may then be easier in a rich sound environment. Complete silence is of course an extreme case, but in total silence the auditory cortex begins to create connections out of thin air, to make up sensory perceptions."

"Then again, the more stimuli there are in the environment, the harder it becomes to focus. In attention disorders such as ADHD, precisely the top-down ability to filter sounds may be lacking," suspects Kauramäki.

In the lipreading tasks Kauramäki did not encounter such a dependency on frequency. Instead, lipreading suppressed the auditory cortex’s ability to react. The reason for this is the neural response of the speech production system.

"The suppressing effect is caused by the adaptation of the areas on the auditory cortex that specialise in speech. Suppressing occurs even when the speech is inaudible – the articulatory gestures of the mouth alone activate parts of the auditory cortex."

For Kauramäki the result suggests that the neural responses of the speech production system can reach the auditory cortex and thus reinforce perception.

"In noisy meetings, for example, it pays off to concentrate on the face of whoever is speaking: lipreading helps in the processing. It may suppress the reaction of the auditory cortex, but the big picture becomes clearer."

Provided by Aalto University

Source: medicalxpress.com

May 24, 2012

(Medical Xpress) — Patients given a clot-busting drug within six hours of a stroke are more likely to make a better recovery than those who do not receive the treatment, new research has found.

The trial was set up in 2000 by the University of Sydney’s Professor Richard Lindley, while he was employed at the University of Edinburgh.

The study of more than 3000 patients is the world’s largest trial of the drug rt-PA and was coordinated at the University of Edinburgh. Since coming to Sydney Medical School in 2003, Professor Lindley has continued as the co-principal investigator of the research.

The findings of the study are published today in The Lancet, alongside an analysis of all other trials of the drug carried out in the past 20 years.

The trial found that following treatment with the drug rt-PA, which is given intravenously to patients who have suffered an acute ischaemic stroke, more patients were able to look after themselves.

"The trial results, together with the updated review, mean that rt-PA can now be offered to a much wider group of patients presenting with stroke", Professor Lindley said.

A patient’s chances of making a complete recovery within six months of a stroke were also increased.

An ischaemic stroke happens when the brain’s blood supply is interrupted by a blood clot. The damage caused can be permanent or fatal.

Researchers now know that for every 1000 patients given rt-PA within three hours of stroke, 80 more will survive and live without help from others than if they had not been given the drug.

The benefits of using rt-PA do come at a price, say researchers. Patients are at risk of death within seven days of treatment because the drug can cause a secondary bleed in the brain. The research team concluded that the benefits were seen in a wide variety of patients, despite the risks.

Stroke experts stress that these mortality figures need to be viewed in the context of deaths from stroke. Without treatment, one third of people who suffer a stroke die, with another third left permanently dependent and disabled.

Researchers say the threat of death and disability means many stroke patients are prepared to take the early risks of being treated with rt-PA to avoid being disabled.

The authors conclude that for those who do not experience bleeding, the drug improves patients’ longer term recovery.

About half of those who took part in the trial were over 80.

"The trial underlines the benefits of treating patients with the drug as soon as possible and provides the first reliable evidence that treatment is effective for those aged 80 and over," Professor Lindley said.

The study also found no reason to restrict use of rt-PA - also known as alteplase - on the basis of how severe a patient’s stroke has been.

Chief investigator Professor Peter Sandercock of the University of Edinburgh’s Centre for Clinical Brain Sciences said: “Our trial shows that it is crucial that treatment is given as fast as possible to all suitable patients.”

Provided by University of Sydney

Source: medicalxpress.com

May 24, 2012

Within the nervous system, a handful of signaling pathways modulate development of a cornucopia of different neuronal subtypes. “Even small alterations in neuron differentiation pathways can disrupt subsequent circuit organization and catalyze the genesis of neurological disorders,” explains Adrian Moore of the RIKEN Brain Science Institute in Wako.

Figure 1: Interplay between Notch signaling and Hamlet activity gives rise to diverse olfactory receptor neurons (ORNs), each with distinct structures and subsets of olfactory receptors (left). The precursor cell (right) divides to yield two daughter cells, one of which undergoes Notch (N)-mediated gene activation. Hamlet (Ham) subsequently resets Notch’s genetic effects, and the absence or subsequent restoration of Notch signaling determines which type of ORN (Naa or Nab) will result from differentiation. Credit: 2012 Adrian Moore, RIKEN Brain Science Institute

Recent work from Moore’s team, which includes Keita Endo of the University of Tokyo, has revealed mechanisms governing this complexity in the fruit fly olfactory system. Within the antennae—the fly equivalent of the nose—it was known that cells called neuronal precursors undergo multiple rounds of ‘asymmetric division’, wherein each resulting daughter cell follows a distinct developmental path, yielding different combinations of olfactory receptor neurons (ORNs). Moore’s team showed specifically that ORN precursors undergo two rounds of division, yielding four different cellular subtypes, three of which will typically mature into ORNs.

Earlier work from Endo showed that the activation or suppression of signaling by the Notch protein helps differentiate these cellular fates, but other factors were clearly involved. Their joint research demonstrated that a second protein, Hamlet, modulates the effects of Notch. 

“This [process] provides an important foundation for all future studies of odorant receptor expression and axon targeting control on the olfactory system,” says Moore. The researchers found that presence or absence of Notch and Hamlet activity plays a central role in establishing the identity of these subtypes, and this in turn determines both the connections formed by the resulting ORNs as well as the subset of olfactory receptor proteins that will be expressed (Fig. 1). 

Moore and Endo’s study also revealed a surprising mode of action for Hamlet. Chromosomal DNA is wrapped around clusters of protein, and chemical changes to those proteins profoundly alter local gene activity—a mechanism called ‘epigenetic regulation’. They found that Hamlet selectively deactivates genes activated by Notch by triggering such changes. This means that immature ORNs produced by division of a Notch-activated cell can essentially be ‘reset’ by Hamlet. The ultimate developmental fate of those cells is then determined, in part, by whether or not they subsequently undergo a new round of Notch activation. 

Moore and colleagues also observed that, beyond simply switching off active Notch genes, Hamlet may define subsets of target genes that can subsequently be reactivated by Notch signaling. “The modifications induced by Hamlet may help establish cell fate by marking gene promoters for use later during differentiation,” says Moore. “This could prove fundamental to understanding the process of neuronal diversification.”

Provided by RIKEN

Source: medicalxpress.com