Doc2-mediated superpriming supports synaptic augmentation

Proceedings of the National Academy of Sciences of the United States of America
Renhao XueEdwin R Chapman

Abstract

Various forms of synaptic plasticity underlie aspects of learning and memory. Synaptic augmentation is a form of short-term plasticity characterized by synaptic enhancement that persists for seconds following specific patterns of stimulation. The mechanisms underlying this form of plasticity are unclear but are thought to involve residual presynaptic Ca2+ Here, we report that augmentation was reduced in cultured mouse hippocampal neurons lacking the Ca2+ sensor, Doc2; other forms of short-term enhancement were unaffected. Doc2 binds Ca2+ and munc13 and translocates to the plasma membrane to drive augmentation. The underlying mechanism was not associated with changes in readily releasable pool size or Ca2+ dynamics, but rather resulted from superpriming a subset of synaptic vesicles. Hence, Doc2 forms part of the Ca2+-sensing apparatus for synaptic augmentation via a mechanism that is molecularly distinct from other forms of short-term plasticity.

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Citations

Jul 10, 2020·Journal of Neurochemistry·Debra AbramovJacqueline Burré
Oct 9, 2019·Scientific Reports·Quentin Bourgeois-JaarsmaAlexander J Groffen
Jan 13, 2021·Proceedings of the National Academy of Sciences of the United States of America·Ermis PofantisThomas Dresbach
Jul 17, 2021·ELife·Shataakshi Dube O'NeilScott H Soderling

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