Dendritic Excitability and Gain Control in Recurrent Cortical Microcircuits.
Dendritic Excitability and Gain Control in Recurrent Cortical Microcircuits.
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DOI：
10.1093/cercor/bhu200
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发表时间：
2015-10
期刊：
影响因子：
--
通讯作者：
Segev I
中科院分区：
文献类型：
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作者：
Hay E;Segev I
新皮质中的第 5 层厚簇状锥体细胞 (TTC) 由于具有高度兴奋的树突，因此在电学方面特别复杂。树突非线性和循环皮层微电路活动在塑造网络响应方面的相互作用在很大程度上是未知的。我们模拟了详细的基于电导的 TTC 模型，这些模型形成了实验发现的互连的循环微电路；该网络嵌入到现实的背景突触活动中。 TTC 微电路显着放大了短暂的丘脑皮质输入；这种皮质增益是由反向传播激活的 N-甲基-d-天冬氨酸去极化和树突反向传播激活的 Ca2+ 尖峰放电介导的，由丘脑激活的体细胞尖峰和源自皮质微电路的局部树突突触输入的同时点燃。令人惊讶的是，TTC 微电路中的树突非线性线性地倍增了丘脑输入——在保持输入选择性的同时放大它们。我们的研究结果表明，树突非线性对于控制 TTC 微电路的增益和计算功能至关重要，TTC 微电路是新皮质的主要输出源。
Layer 5 thick tufted pyramidal cells (TTCs) in the neocortex are particularly electrically complex, owing to their highly excitable dendrites. The interplay between dendritic nonlinearities and recurrent cortical microcircuit activity in shaping network response is largely unknown. We simulated detailed conductance-based models of TTCs forming recurrent microcircuits that were interconnected as found experimentally; the network was embedded in a realistic background synaptic activity. TTCs microcircuits significantly amplified brief thalamocortical inputs; this cortical gain was mediated by back-propagation activated N-methyl-d-aspartate depolarizations and dendritic back-propagation-activated Ca2+ spike firing, ignited by the coincidence of thalamic-activated somatic spike and local dendritic synaptic inputs, originating from the cortical microcircuit. Surprisingly, dendritic nonlinearities in TTCs microcircuits linearly multiplied thalamic inputs—amplifying them while maintaining input selectivity. Our findings indicate that dendritic nonlinearities are pivotal in controlling the gain and the computational functions of TTCs microcircuits, which serve as a dominant output source for the neocortex.