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Doc2-mediated superpriming supports synaptic augmentation
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DOI：10.1073/pnas.1802104115.png)
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摘要
En 中文
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.
Keyword:
short-term plasticity
synaptic augmentation
Doc2
munc13
superpriming
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期刊
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IF:
9.1
论文数:
10.8W
被引数:
73.5W
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引用论文
A C1-C2 Module in Munc13 Inhibits Calcium-Dependent Neurotransmitter ReleaseMunc13中的C1-C2模块抑制钙依赖性神经递质的释放.png)
NEURONOAAI
NEURONIF15
OAAI分享收藏Structural elements that underlie Doc2β function during asynchronous synaptic transmission异步突触传递过程中Doc2β 功能的基础结构元素OAAI
OAAI分享收藏ASYNCHRONOUS RELEASE OF SYNAPTIC VESICLES DETERMINES THE TIME-COURSE OF THE AMPA RECEPTOR-MEDIATED EPSCNEURONOAAI
NEURONIF15
OAAI分享收藏Doc2B acts as a calcium sensor for vesicle priming requiring synaptotagmin-1, Munc13-2 and SNAREsELIFEOAAI
ELIFEIF0
OAAI分享收藏
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