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电压门控Ca2+通道的阈下突触激活介导局部Ca2+流入海马锥体神经元的树突。

Subthreshold synaptic activation of voltage-gated Ca2+ channels mediates a localized Ca2+ influx into the dendrites of hippocampal pyramidal neurons.

作者信息

Magee J C, Christofi G, Miyakawa H, Christie B, Lasser-Ross N, Johnston D

机构信息

Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, USA.

出版信息

J Neurophysiol. 1995 Sep;74(3):1335-42. doi: 10.1152/jn.1995.74.3.1335.

Abstract
  1. Whole cell recordings and high-speed fluorescence imaging were used to investigate the spatial and temporal characteristics of Ca2+ influx during synaptic activity in hippocampal CA1 pyramidal neurons. Brief, subthreshold trains of synaptic potentials elicited by Schaffer collateral stimulation produced transient increases in [Ca2+]i in the apical dendrites near the site of synaptic input. The rises in [Ca2+]i were not due to Ca2+ entry through N-methyl-D-aspartate (NMDA)-activated or non-NMDA-activated glutamate channels, but were reduced by low concentrations of Ni2+. Hyperpolarizing prepulses caused an increase in the synaptically evoked Ca2+ transients, whereas strong hyperpolarization during the train prevented the rise in [Ca2+]i. The data suggest that subthreshold synaptic activity can open low-voltage-activated (T-type) Ca2+ channels and produce a local increase in intradendritic [Ca2+]. Such local increases in [Ca2+]i may be important for modulating the strength of synaptic connections.
摘要
  1. 全细胞记录和高速荧光成像被用于研究海马CA1锥体神经元突触活动期间Ca2+内流的时空特征。由Schaffer侧支刺激引发的短暂、阈下突触电位序列在突触输入部位附近的顶端树突中产生了[Ca2+]i的瞬时增加。[Ca2+]i的升高并非由于通过N-甲基-D-天冬氨酸(NMDA)激活或非NMDA激活的谷氨酸通道的Ca2+内流,而是被低浓度的Ni2+所降低。超极化预脉冲导致突触诱发的Ca2+瞬变增加,而在序列期间的强超极化则阻止了[Ca2+]i的升高。数据表明阈下突触活动可打开低电压激活(T型)Ca2+通道并在树突内产生局部[Ca2+]增加。这种[Ca2+]i的局部增加可能对调节突触连接强度很重要。

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