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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
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Home | Pregnancy Timeline | News Alerts |News Archive Sep 23, 2013

 

Two neighboring brain cells "talk" to one another by sending signals across a gap called a synapse. The more active the synapse during development, U-M researchers found, the more a protein called SIRP-alpha is cut loose from one cell, travels to the other, and helps stabilize the synapse for the future.







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Building the best brain

Researchers show how brain cell connections get cemented early in life. Research on synapse stabilization could aid understanding of autism, schizophrenia, intellectual disability.

When we’re born, our brains aren’t very organized. Every brain cell talks to lots of other nearby cells, sending and receiving signals across connections called synapses.

Two neighboring brain cells "talk" to one another by sending signals across a gap called a synapse. The more active the synapse during development, U-M researchers found, the more a protein called SIRP is cut loose from one cell, travels to the other, and helps stabilize the synapse for the future.
But as we grow and learn, things get a bit more stable. The brain pathways that will serve us our whole lives start to organize, and less-active, inefficient synapses shut down.

But why and how does this happen? And what happens when it doesn’t go normally? New research from the University of Michigan Medical School may help explain.

In a new paper in Nature Neuroscience, a team of U-M neuroscientists reports important findings about how brain cells called neurons keep their most active connections with other cells, while letting other synapses lapse.

Specifically, they show that SIRP alpha, a protein found on the surface of various cells throughout the body, appears to play a key role in the process of cementing the most active synaptic connections between brain cells. The research, done in mouse brains, was funded by the National Institutes of Health and several foundations.

The findings boost understanding of basic brain development – and may aid research on conditions like autism, schizophrenia, epilepsy and intellectual disability, all of which have some basis in abnormal synapse function.


“For the brain to be really functional, we need to keep the most active and most efficient connections. So, during development it’s crucial to establish efficient connections, and to eliminate inactive ones. We have identified a key molecular mechanism that the brain uses to stabilize and maturate the most active connections.”

Hisashi Umemori, M.D., Ph.D., senior author, research assistant professor at U-M’s Molecular and Behavioral Neuroscience Institute and assistant professor of biological chemistry in the Medical School.


Umemori says the new findings on SIRP alpha grew directly out of previous work on competition between neurons, which enables the most active ones to become part of pathways and circuits. (Read more on this research)

The team suspected that there must be some sort of signal between the two cells on either side of each synapse -- something that causes the most active synapses to stabilize. So they set out to find out what it was.


SIRP-rise findings

The scientists had previously shown that SIRP-alpha was involved in some way in a neuron’s ability to form a presynaptic nerve terminal – an extension of the cell that reaches out toward a neighboring cell — and can send the chemical signals that brain cells use to talk to one another.

SIRP-alpha is also already known to serve an important function in the rest of the body — essentially helping normal cells tell the immune system not to attack them. It may also help cancer cells evade detection by the immune system’s watchdogs.


In the new study, the team studied SIRP alpha function in the brain – and started to understand its role in synapse stabilization. They focused on the hippocampus, a region of the brain very important to learning and memory.

Through a range of experiments, they showed that when a brain cell receives signals from a neighboring cell across a synapse, it actually releases SIRP-alpha into the space between the cells. It does this through the action of molecules inside the cell – called CaMK and MMP – that act like molecular scissors, cutting a SIRP-alpha protein in half so that it can float freely away from the cell.

The part of the SIRP-alpha protein that floats into the synapse “gap” latches on to a receptor on the other side, called a CD47 receptor. This binding, in turn, appears to tell the cell that the signal it sent earlier was indeed received – and that the synapse is a good one. So, the cell brings more chemical signaling molecules down that way, and releases them into the synapse.

As more and more nerve messages travel between the “sending” and “receiving” cells on either side of that synapse, more SIRP-alpha gets cleaved, released into the synapse, and bound to CD47.

The researchers believe this repeated process is what helps the cells determine which synapses to keep – and which to let wither.

Umemori says the team next wants to look at what happens when SIRP-alpha doesn’t get cleaved as it should – and at what’s happening in cells when a synapse gets eliminated.

“This step of shedding SIRP-alpha must be critical to developing a functional neural network,” Umemori adds. “And if it’s not done well, disease or disorders may result. Perhaps we can use this knowledge to treat diseases caused by defects in synapse formation.”


He points out that the gene for the CD47 receptor is found in the same general area of our DNA as several genes suspected to be involved in schizophrenia.


Abstract
Formation of appropriate synaptic connections is critical for proper functioning of the brain. After initial synaptic differentiation, active synapses are stabilized by neural activity-dependent signals to establish functional synaptic connections. However, the molecular mechanisms underlying activity-dependent synapse maturation remain to be elucidated. Here we show that activity-dependent ectodomain shedding of signal regulatory protein-α (SIRPα) mediates presynaptic maturation. Two target-derived molecules, fibroblast growth factor 22 and SIRPα, sequentially organize the glutamatergic presynaptic terminals during the initial synaptic differentiation and synapse maturation stages, respectively, in the mouse hippocampus. SIRPα drives presynaptic maturation in an activity-dependent fashion. Remarkably, neural activity cleaves the extracellular domain of SIRPα, and the shed ectodomain in turn promotes the maturation of the presynaptic terminal. This process involves calcium/calmodulin-dependent protein kinase, matrix metalloproteinases and the presynaptic receptor CD47. Finally, SIRPα-dependent synapse maturation has an impact on synaptic function and plasticity. Thus, ectodomain shedding of SIRPα is an activity-dependent trans-synaptic mechanism for the maturation of functional synapses.

In addition to Umemori, the research group includes: Anna Toth, Akiko Terauchi, Lily Y. Zhang, Erin Johnson-Venkatesh and David J Larsen of the Molecular & Behavioral Neuroscience Institute, and Michael A. Sutton, Ph.D., an assistant professor in both MBNI and the Department of Molecular & Integrative Physiology.

Funding: The researchers used the Medical School’s Transgenic Animal Model Core and cores of the U-M Center for Organogenesis. The research was funded by the Ester A. & Joseph Klingenstein Fund, the Edward Mallinckrodt Jr. Foundation, the March of Dimes Foundation, the Whitehall Foundation and National Institutes of Health (MH091429, NS070005 and MH092614 )

Reference: Nature Neuroscience, Advance Online Publication, doi:10.1038/nn.3516, http://www.nature.com/doifinder/10.1038/nn.3516

Original press releas: http://www.uofmhealth.org/news/archive/201309/building-best-brain-u-m-researchers-show-how-brain-cell