Study identifies new key role for astrocytes in memory and learning.


Glial cells are immune cells found in the brain which do not participate directly in synaptic interactions or electrical signaling like nerve cells, although their supportive functions help define synaptic contacts and maintain the signaling abilities of neurons.   Astrocytes are specialized glial cells which outnumber neurons by over fivefold, with astrocytic roles and involvement in neurological disease still being discovered.  Now, a study from researchers at UC Riverside shows that when astrocytes over produce a protein called ephrin-B1, the ability to retain memory weakens.  The team state their data suggests that too much ephrin-B1 can damage neurons and remove synapses, with such synapse loss seen in neurodegenerative disorders such as Alzheimer’s disease.  The new study is published in the Journal of Neuroscience.

Previous studies show that astrocytes regulate synapse formation and functions, making astrocytes an attractive target for regulating neuronal circuits. Abnormal astrocyte-neuronal interactions are also implicated in neurodevelopmental disorders and diseases associated with impaired learning and memory. However, not a lot is known about astrocytic mechanisms which regulate learning and memory.  The current study in mice shows that overproduction of ephrin-B1 in astrocytes can lead to impaired retention of contextual memory.

The current study observes mouse cell behavior in a petri dish to show that astrocytes attack synapses when ephrin-B1 is over-expressed, suggesting that glial-neuronal interactions influence learning and memory.  Results show that when levels of ephrin-B1 are artificially increased in mice they can’t remember a behaviour they’ve recently learned.  Data findings in cell culture studies show that when neurons are added to astrocytes that over-expressed ephrin-B1, synapse removal is observed, with astrocytes devouring the synapses.

Results show that when levels of ephrin-B1 decrease more synapses are formed leading to improved learning; the astrocytes, in this case, are not able to attach to the synapses.  The lab hypothesize that the overproduction of ephrin-B1 can be a novel mechanism by which unwanted synapses are removed in the healthy brain, with excessive removal leading to neurodegeneration.  They go on to add that while the research was done on a mouse model, the results are applicable in humans whose astrocytes also produce ephrin-B1.

The team surmise that their study demonstrates that astrocytic ephrin-B1 regulates long-term contextual memory by restricting new synapse formation in the adult hippocampus.  For the future, the researchers state these findings establish a foundation for studies of astrocytic regulation of synaptogenesis to guide the development of clinical applications for a variety of neurological disorders.

Source: University of California – Riverside

 

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