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温度对海兔神经元中起搏器产生、膜电位和临界放电阈值的影响。

Temperature effects on pacemaker generation, membrane potential, and critical firing threshold in Aplysia neurons.

作者信息

Carpenter D O

出版信息

J Gen Physiol. 1967 Jul;50(6):1469-84. doi: 10.1085/jgp.50.6.1469.

Abstract

Temperature increases cause a regular and reproducible increase in the frequency of generation of pacemaker potentials in most Aplysia neurons specialized for this type of activity which can only be explained as a direct stimulating effect of temperature upon the ionic mechanisms responsible for pacemaker potentials. At the same time all cells in the visceral ganglion undergo a membrane potential hyperpolarization of approximately 1-2 mv/ degrees C warmed. In spite of the marked variation in resting membrane potential the critical firing threshold remains at a constant membrane potential level at all temperatures in the absence of accommodative changes. The temperature-frequency curves of all types of cells are interpreted as a result of the interaction between the effects of temperature on the pacemaker-generating mechanism and resting membrane potential. Previous observations on the effects of temperature on excitability of mammalian neurons suggest that other types of neurons may undergo similar marked shifts in resting membrane potential with temperature variation.

摘要

温度升高会使大多数专门进行此类活动的海兔神经元中起搏器电位的产生频率出现规律性且可重复的增加,这只能解释为温度对负责起搏器电位的离子机制产生直接刺激作用。与此同时,内脏神经节中的所有细胞在温度每升高1摄氏度时会经历约1 - 2毫伏的膜电位超极化。尽管静息膜电位存在显著变化,但在没有适应性变化的情况下,临界放电阈值在所有温度下都保持在恒定的膜电位水平。所有类型细胞的温度 - 频率曲线被解释为温度对起搏器产生机制和静息膜电位的影响之间相互作用的结果。先前关于温度对哺乳动物神经元兴奋性影响的观察表明,其他类型的神经元可能会随着温度变化在静息膜电位上发生类似的显著变化。

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