Mechanisms underlying the rapid induction and sustained expression of synaptic homeostasis
Mechanisms underlying the rapid induction and sustained expression of synaptic homeostasis
复制标题
DOI：
10.1016/j.neuron.2006.09.029
复制
发表时间：
2006-11-22
期刊：
影响因子：
16.2
通讯作者：
Davis, Graeme W.
中科院分区：
文献类型：
--
作者：
Frank, C. Andrew;Kennedy, Matthew J.;Davis, Graeme W.
稳态信号系统被认为与神经可塑性机制相结合，以实现稳定而灵活的神经回路。然而，稳态信号传导的时间过程、分子设计和实现仍然不清楚。在这里，我们证明了突触前神经递质释放的稳态增加可以在突触后谷氨酸受体阻断后几分钟内诱导。突触稳态的快速诱导独立于新的蛋白质合成，并且不需要诱发的神经传递，这表明自发量子释放事件的功效的变化足以触发突触稳态的诱导。最后，突触稳态的快速诱导和持续表达都被突变阻断，突变破坏了由杂音编码的突触前Ca（v）2.1钙通道的孔形成亚基。这些数据证实了突触内稳态的突触前表达，并暗示突触前Ca（v）2.1在稳态逆行信号系统中。
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.