Functional and Pathological Influence of Hypothermia on Spike Activity of Cortical Neurons

Y. Mednikova, N. M. Zakharova, N. Pasikova
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Abstract

In sensorimotor cortical slices of guinea pig using local iontophoretic application of glutamate to the soma and dendrites it was found that a decrease of temperature of incubating fluid from 34 to 21°C - 22°C changes the somatic responses to the local injection of glutamate to the dendritic loci, while the responses to iontophoretic application of glutamate to the soma remain unchanged. Hypothermic changes in reactivity to dendritic stimulation start below 30°C and coincide with changes in the spontaneous activity of neurons, both in the direction of increasing and decreasing the frequency of firing in different nerve cells. On hypothermic decrease of spontaneous activity, the latencies of evoked dendritic responses on the soma became more longer, while on hypothermic increase of firing level, somatic spike responses to iontophoretic application of glutamate to dendritic loci appeared with shorter latencies. Hypothermic changes in the physiological parameters of neurons were accompanied by a drop in spike amplitude at the same temperature and with its further decrease. At the same time, there was a decrease of spike reaction to iontophoretic application of acetylcholine below 30°. It is proposed that the reason for hypothermic changes of neuronal activity is decreasing rate of M-cholinergic process at 27°C - 29°C which leads to opening K+ channels of neuronal membranes and hence to attenuation of conductive function of dendrites and to imbalance of K+ ion homeostasis. Peculiarities of hypothermic regulation of neuronal spike activity depend on individual functional properties of cortical neurons.
低温对皮质神经元尖峰活动的功能和病理影响
短句来源对谷氨酸局部离子注入豚鼠体细胞和树突的感觉运动皮层切片研究发现,当孵卵液温度从34℃降至21℃~ 22℃时,细胞对谷氨酸局部注入树突位点的反应发生改变,而对谷氨酸局部离子注入体细胞的反应保持不变。树突刺激反应性的低温变化始于30°C以下,与神经元自发活动的变化一致,在不同的神经细胞中都有增加和减少放电频率的方向。当自发活动降低时,诱发的树突反应潜伏期变长,而当放电水平升高时,谷氨酸对树突位点的离子吸附引起的体突反应潜伏期变短。神经元生理参数的低温变化伴随着相同温度下的峰值幅度下降,并进一步降低。与此同时,在30°以下,乙酰胆碱离子吸附后的刺突反应减弱。提出神经元活动低温变化的原因是在27℃- 29℃时m -胆碱能过程速率降低,导致神经元膜K+通道打开,从而导致树突传导功能衰减,K+离子稳态失衡。神经元尖峰活动的低温调节特性取决于皮质神经元的个体功能特性。
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