Temperature effects on pacemaker generation, membrane potential, and critical firing threshold in Aplysia neurons.
Temperature effects on pacemaker generation, membrane potential, and critical firing threshold in Aplysia neurons.
复制标题
DOI：
10.1085/jgp.50.6.1469
复制
发表时间：
1967-07
期刊：
影响因子：
--
通讯作者：
Carpenter DO
中科院分区：
文献类型：
--
作者：
Carpenter DO
温度升高会导致大多数专门从事这种活动的失智症神经元产生起搏电位的频率出现规律性和可重复性的增加，这只能解释为温度对负责起搏电位的离子机制的直接刺激作用。与此同时，内脏神经节中的所有细胞都经历了约1-2 mV/°C的膜电位超极化。尽管在静息膜电位的显着变化的临界放电阈值保持在一个恒定的膜电位水平在所有温度下的情况下，不发生的变化。所有类型的细胞的温度-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的相互作用的结果。以前的观察温度对哺乳动物神经元兴奋性的影响表明，其他类型的神经元可能会经历类似的显着变化，在静息膜电位与温度的变化。
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/°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.