Mechanisms underlying the rapid induction and sustained expression of synaptic homeostasis

被引：294

作者：

Frank, C. Andrew ^{[1
]}

Kennedy, Matthew J. ^{[1
]}

Goold, Carleton P. ^{[1
]}

Marek, Kurt W. ^{[1
]}

Davis, Graeme W. ^{[1
]}

机构：

[1] Univ Calif San Francisco, Dept Biochem & Biophys, Neurosci Program, San Francisco, CA 94158 USA

来源：

NEURON | 2006年 / 52卷 / 04期

关键词：

D O I：

10.1016/j.neuron.2006.09.029

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Homeostatic signaling systems are thought to interface with the mechanisms of neural plasticity to achieve stable yet flexible neural circuitry. However, the time course, molecular design, and implementation of homeostatic signaling remain poorly defined. Here we demonstrate that a homeostatic increase in presynaptic neurotransmitter release can be induced within minutes following postsynaptic glutamate receptor blockade. The rapid induction of synaptic homeostasis is independent of new protein synthesis and does not require evoked neurotransmission, indicating that a change in the efficacy of spontaneous quantal release events is sufficient to trigger the induction of synaptic homeostasis. Finally, both the rapid induction and the sustained expression of synaptic homeostasis are blocked by mutations that disrupt the pore-forming subunit of the presynaptic Ca(v)2.1 calcium channel encoded by cacophony. These data confirm the presynaptic expression of synaptic homeostasis and implicate presynaptic Ca(v)2.1 in a homeostatic retrograde signaling system.

引用

页码：663 / 677

页数：15

共 52 条

[11] Postsynaptic PKA controls quantal size and reveals a retrograde signal that regulates presynaptic transmitter release in Drosophila [J].