A model of spike initiation in neocortical pyramidal neurons
A model of spike initiation in neocortical pyramidal neurons
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DOI：
10.1016/0896-6273(95)90020-9
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发表时间：
1995-12-01
期刊：
影响因子：
16.2
通讯作者：
Sejnowski, TJ
中科院分区：
文献类型：
--
作者：
Mainen, ZF;Joerges, J;Sejnowski, TJ
新皮质锥体细胞具有电压依赖性树突状钠通道，其促进动作电位向树突树的传播，但矛盾的是可能无法产生树突棘波。构建了一个生物物理模型，以使这些观察结果与已知的解剖学和生理学特性相一致。当树突和体细胞钠通道密度与电生理学测量相兼容的轴突初始段中的高得多的密度相结合，然后，无论刺激的部位，尖峰起始于初始段，随后侵入树突。较低的初始节段阈值产生于高电流密度和与索马的电隔离。树突状通道启动尖峰的失败是由于失活和源负载的考虑，这更有利于反向传播尖峰的传导。
Neocortical pyramidal cells possess voltage-dependent dendritic sodium channels that promote propagation of action potentials into the dendritic tree but paradoxically may fail to originate dendritic spikes. A biophysical model was constructed to reconcile these observations with known anatomical and physiological properties. When dendritic and somatic sodium channel densities compatible with electrophysiological measurements were combined with much higher densities in the axon initial segment then, regardless of the site of stimulation, spikes initiated at the initial segment and subsequently invaded the dendrites. The lower initial segment threshold arose from high current density and electrical isolation from the soma. Failure of dendritic channels to initiate spikes was due to inactivation and source-load considerations, which were more favorable for conduction of back-propagated spikes.