The ionic mechanism of gamma resonance in rat striatal fast-spiking neurons
The ionic mechanism of gamma resonance in rat striatal fast-spiking neurons
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DOI：
10.1152/jn.00280.2011
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发表时间：
2011-12-01
影响因子：
2.5
通讯作者：
Wilson, Charles J.
中科院分区：
文献类型：
--
作者：
Sciamanna, Giuseppe;Wilson, Charles J.
首页--期刊主要分类--期刊细介绍--期刊题录与文摘大鼠纹状体快脉冲神经元伽马共振的离子机制。神经生理学杂志106：2936-2949,2011。2011年8月31日首次出版；DOI：10.1152/jn.00280.2011。-伽马频率范围内和体内的切片中的条纹快速尖峰(FS)细胞经常与场电位中的伽马振荡锁相。我们研究了16-23日龄大鼠脑片中这些细胞的放电模式，以确定它们的伽马共振机制。纹状体FS细胞的共振表现为重复放电的最低频率。在血流底，细胞发出一对动作电位或由停顿隔开的一对动作电位，瞬时放电频率平均为44个峰/S。持续放电的最低频率也是导致放电模式卡顿的原因。在每一次射击过程中调整射击速度，并在射击降至最低可持续速度时终止爆炸。在用四乙基铵(0.1-1 mm)阻断Kv3电流后，共振和口吃仍在继续。伽玛共振和口吃都强烈依赖于KV1电流。用树突状毒素I(100 NM)阻断KV1通道，可完全消除卡顿放电模式，显著降低最小放电频率，消除伽马频段亚阈值振荡，减缓尖峰频率适应。共振的丧失可以归因于尖峰阈值附近钾电流的减少和一个固定的尖峰阈值的出现。KV1通道的失活加上最小的放电频率可以解释口吃的放电模式。由该通道赋予的共振特性被证明足以解释它们对伽马频率输入的锁相，就像在活体中看到的那样。
Sciamanna G, Wilson CJ. The ionic mechanism of gamma resonance in rat striatal fast-spiking neurons. J Neurophysiol 106: 2936-2949, 2011. First published August 31, 2011; doi: 10.1152/jn.00280.2011.-Striatal fast-spiking (FS) cells in slices fire in the gamma frequency range and in vivo are often phase-locked to gamma oscillations in the field potential. We studied the firing patterns of these cells in slices from rats ages 16-23 days to determine the mechanism of their gamma resonance. The resonance of striatal FS cells was manifested as a minimum frequency for repetitive firing. At rheobase, cells fired a doublet of action potentials or doublets separated by pauses, with an instantaneous firing rate averaging 44 spikes/s. The minimum rate for sustained firing was also responsible for the stuttering firing pattern. Firing rate adapted during each episode of firing, and bursts were terminated when firing was reduced to the minimum sustainable rate. Resonance and stuttering continued after blockade of Kv3 current using tetraethylammonium (0.1-1 mM). Both gamma resonance and stuttering were strongly dependent on Kv1 current. Blockade of Kv1 channels with dendrotoxin-I (100 nM) completely abolished the stuttering firing pattern, greatly lowered the minimum firing rate, abolished gamma-band subthreshold oscillations, and slowed spike frequency adaptation. The loss of resonance could be accounted for by a reduction in potassium current near spike threshold and the emergence of a fixed spike threshold. Inactivation of the Kv1 channel combined with the minimum firing rate could account for the stuttering firing pattern. The resonant properties conferred by this channel were shown to be adequate to account for their phase-locking to gamma-frequency inputs as seen in vivo.