Study identifies new key role for astrocytes in memory and learning.
Glial cells are immune cells found in the brain not directly involved in synaptic interactions or electrical signaling, although their supportive functions are known to play a crucial role in defining synaptic contacts and maintaining the signaling abilities of neurons. Astrocytes are specialized glial cells thought to outnumber neurons by at least fivefold, with astrocytic roles and involvement in neurological disease still being discovered. Now, a study from researchers at UC Riverside demonstrates the ability to retain memory weakens when astrocytes overproduce a protein called ephrin-B1. The team states their data suggests too much ephrin-B1 can damage neurons and remove synapses, with similar synapse loss seen in neurodegenerative disorders such as Alzheimer’s disease. The new study is published in the Journal of Neuroscience.
Previous studies show astrocytes regulate synapse formation and functions, making these cells a logical hypothetical 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 regulating learning and memory. The current study in mice shows the overproduction of ephrin-B1 in astrocytes can lead to impaired retention of contextual memory.
The current study observes cellular behavior in mice in vitro to show astrocytes attack synapses when ephrin-B1 is over-expressed, suggesting these glial-neuronal interactions influence learning and memory. Results show when levels of ephrin-B1 are artificially increased in mice they can’t remember a behavior they’ve recently learned. Data findings using in vitro studies show when neurons are added to astrocytes that over-expressed ephrin-B1, synapse removal is observed, with astrocytes devouring the synapses.
Results show when levels of ephrin-B1 decrease more synapses are formed leading to improved learning with astrocytes unable to attach to the synapses. The lab posits the overproduction of ephrin-B1 can be a novel mechanism capable of removing unwanted synapses in the healthy brain, with excessive removal leading to neurodegeneration. They go on to add while the research was done using a mouse model, the results are applicable in humans whose astrocytes also produce ephrin-B1.
The team surmises their study demonstrates 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.
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