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大鼠纹状体中快速棘突神经元 γ 共振的离子机制。

The ionic mechanism of gamma resonance in rat striatal fast-spiking neurons.

机构信息

Laboratory of Neurophysiology and Plasticity, Santa Lucia Foundation IRCCS, Rome, Italy.

出版信息

J Neurophysiol. 2011 Dec;106(6):2936-49. doi: 10.1152/jn.00280.2011. Epub 2011 Aug 31.

DOI:10.1152/jn.00280.2011
PMID:21880937
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3234086/
Abstract

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.

摘要

纹状体快速放电 (FS) 细胞在切片中以伽马频率范围放电,并且在体内通常与场电位中的伽马振荡相位锁定。我们研究了来自 16-23 天大的大鼠切片中这些细胞的放电模式,以确定它们伽马共振的机制。纹状体 FS 细胞的共振表现为重复放电的最小频率。在电流阈值时,细胞发射双脉冲动作电位或双脉冲之间有停顿,瞬时放电率平均为 44 个脉冲/s。持续放电的最小速率也负责产生口吃的放电模式。在每次放电期间,放电率都会适应,并且当放电率降低到最小可持续速率时,爆发就会终止。在使用四乙铵(0.1-1 mM)阻断 Kv3 电流后,共振和口吃仍会继续。伽马共振和口吃都强烈依赖于 Kv1 电流。使用树突毒素-I(100 nM)阻断 Kv1 通道会完全消除口吃的放电模式,大大降低最小放电率,消除伽马频带阈下振荡,并减缓尖峰频率适应。共振的丧失可以归因于尖峰阈值附近钾电流的减少和固定尖峰阈值的出现。Kv1 通道的失活与最小放电率相结合,可以解释口吃的放电模式。该通道赋予的共振特性足以解释它们在体内与伽马频率输入的相位锁定。

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