Synchronized gamma-frequency inhibition in neocortex depends on excitatory-inhibitory interactions but not electrical synapses.
Synchronized gamma-frequency inhibition in neocortex depends on excitatory-inhibitory interactions but not electrical synapses.
复制标题
新皮质中的同步伽马频率抑制取决于兴奋-抑制相互作用，而不是电突触。
DOI：
10.1152/jn.00071.2016
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发表时间：
2016
影响因子：
2.5
通讯作者：
Connors,BarryW
中科院分区：
文献类型：
--
作者：
Neske,GarrettT;Connors,BarryW
突触抑制在大脑皮层尖峰活动的精确定时中起着至关重要的作用。伽马（30-80 Hz）范围内的同步、节律性抑制活动被认为对活跃的信息处理新皮层特别重要，但引起同步抑制的电路机制尚不确定。特别是，相互抑制连接、兴奋-抑制相互作用和电突触对抑制性中间神经元之间精确锋电位同步的相对贡献还没有得到很好的理解。在这里，我们描述了小鼠桶皮层在体外的实验，因为它自发地产生缓慢（<1 Hz）的振荡（向上和向下状态）。在Up状态下，抑制性突触后电流（IPSC）以伽马频率产生，并且比相邻锥体细胞之间的兴奋性突触后电流（EPSC）更同步。此外，尖峰在同型对的中间神经元更同步比对锥体细胞。比较connexin 36基因敲除和野生型动物，我们发现，电突触作出最小的贡献，同步抑制在Up状态。对单个锥体细胞中EPSC和IPSC之间的延迟的估计表明，兴奋通常先于抑制几毫秒。最后，在没有兴奋的情况下，不同中间神经元亚型的紧张性光遗传学激活导致锥体神经元对中IPSC的仅弱同步。我们的研究结果表明，相位兴奋性输入是必不可少的抑制性中间神经元在Up状态的同步尖峰和电突触发挥最小的作用。
Synaptic inhibition plays a crucial role in the precise timing of spiking activity in the cerebral cortex. Synchronized, rhythmic inhibitory activity in the gamma (30–80 Hz) range is thought to be especially important for the active, information-processing neocortex, but the circuit mechanisms that give rise to synchronized inhibition are uncertain. In particular, the relative contributions of reciprocal inhibitory connections, excitatory-inhibitory interactions, and electrical synapses to precise spike synchrony among inhibitory interneurons are not well understood. Here we describe experiments on mouse barrel cortex in vitro as it spontaneously generates slow (<1 Hz) oscillations (Up and Down states). During Up states, inhibitory postsynaptic currents (IPSCs) are generated at gamma frequencies and are more synchronized than excitatory postsynaptic currents (EPSCs) among neighboring pyramidal cells. Furthermore, spikes in homotypic pairs of interneurons are more synchronized than in pairs of pyramidal cells. Comparing connexin36 knockout and wild-type animals, we found that electrical synapses make a minimal contribution to synchronized inhibition during Up states. Estimations of the delays between EPSCs and IPSCs in single pyramidal cells showed that excitation often preceded inhibition by a few milliseconds. Finally, tonic optogenetic activation of different interneuron subtypes in the absence of excitation led to only weak synchrony of IPSCs in pairs of pyramidal neurons. Our results suggest that phasic excitatory inputs are indispensable for synchronized spiking in inhibitory interneurons during Up states and that electrical synapses play a minimal role.