Regulation of interneuron excitability by gap junction coupling with principal cells.
Regulation of interneuron excitability by gap junction coupling with principal cells.
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DOI：
10.1038/nn.3569
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发表时间：
2013-12
影响因子：
25
通讯作者：
Trussell, Laurence O.
中科院分区：
文献类型：
--
作者：
Apostolides, Pierre F.;Trussell, Laurence O.
抑制性中间神经元的电耦合可以使多个神经元的活动同步，从而提高对主要细胞靶点的抑制的可靠性。目前尚不清楚主细胞的下游活动是否控制了这种抑制网络的兴奋性。在膜片钳记录中，我们发现耳蜗背核的兴奋性投射神经元(梭形细胞)和抑制性星状中间神经元通过含有缝隙连接蛋白36的缝隙连接形成电耦合网络。值得注意的是，星状细胞与梭形细胞的偶联程度高于与其他星状细胞的偶联程度。这种异源偶联在功能上是不对称的，偏向于从主细胞到中间神经元的电传递。光基因激活的梭形细胞群体可靠地增强了神经元间的兴奋性，并对星状细胞的突触后靶点产生GABA能抑制，而梭形细胞棘波序列后的深层超极化在数百毫秒内有效地抑制了星状细胞。因此，神经元间网络的兴奋性是由主细胞中不同的活动时期双向控制的。
Electrical coupling of inhibitory interneurons can synchronize activity across multiple neurons, thereby enhancing the reliability of inhibition onto principal cell targets. It is unclear whether downstream activity in principal cells controls the excitability of such inhibitory networks. Using paired patch-clamp recordings, we show that excitatory projection neurons (fusiform cells) and inhibitory stellate interneurons of the dorsal cochlear nucleus form an electrically coupled network via connexin36-containing gap junctions. Remarkably, stellate cells were more strongly coupled to fusiform cells than to other stellate cells. This heterologous coupling was functionally asymmetric, biasing electrical transmission from principal cell to interneuron. Optogenetically-activated populations of fusiform cells reliably enhanced interneuron excitability and generated GABAergic inhibition onto postsynaptic targets of stellate cells, whereas deep afterhyperpolarizations following fusiform cell spike trains potently inhibited stellate cells over several hundred milliseconds. Thus, the excitability of an interneuron network is bi-directionally-controlled by distinct epochs of activity in principal cells.
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