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活动诱导的小脑深部核团神经元细胞内钙浓度升高。

Activity induced elevations of intracellular calcium concentration in neurons of the deep cerebellar nuclei.

作者信息

Muri R, Knöpfel T

机构信息

Brain Research Institute, University of Zürich, Switzerland.

出版信息

J Neurophysiol. 1994 Jan;71(1):420-8. doi: 10.1152/jn.1994.71.1.420.

DOI:10.1152/jn.1994.71.1.420
PMID:8158239
Abstract
  1. Depolarization-induced changes in the cytosolic free calcium concentration ([Ca2+]i) were examined in slice-cultured neurons of the deep cerebellar nuclei by combined intracellular and multisite fura-2 recording techniques. 2. Firing of tetrodotoxin (TTX)-sensitive action potentials induced by depolarizing current pulses caused large elevations in somatic as well as proximal dendritic [Ca2+]i. In the dendrites, rise and decay times of [Ca2+]i were faster than in the soma. [Ca2+]i changes associated with depolarizations to < or = -40 mV in the presence of TTX were small compared with changes induced by Na+ spike firing, suggesting that Ca2+ influx through high voltage-activated Ca2+ channels is a major cause for Na+ spike-associated [Ca2+]i increases. 3. During sustained Na+ spike firing at a constant frequency (> 20 Hz), [Ca2+]i approached a constant level, after approximately 1 s in the dendrites and 2 s in the soma, respectively. The amplitude of the attained level was positively correlated with the firing frequency. We suggest that during tonic activity [Ca2+]i reaches a steady state determined by Ca2+ influx and extrusion. 4. TTX-resistant plateau potentials caused substantially greater [Ca2+]i increases in the dendrites than in the soma. In the dendrites, plateau-associated Ca2+ transients were comparable in amplitude to Ca2+ transients triggered by short (50 ms) Na+ spike trains, in the soma, they were considerably smaller. 5. Low-threshold spikes (LTSs) in association with a burst of Na+ spikes induced a sharp increase in [Ca2+]i both in the soma and in dendrites.(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 运用细胞内与多部位fura - 2记录技术相结合的方法,研究了深小脑核团切片培养神经元中去极化诱导的胞质游离钙浓度([Ca2+]i)变化。2. 去极化电流脉冲诱发的河豚毒素(TTX)敏感动作电位发放,导致胞体以及近端树突的[Ca2+]i大幅升高。在树突中,[Ca2+]i的上升和衰减时间比胞体更快。在TTX存在的情况下,与去极化至≤ -40 mV相关的[Ca2+]i变化,与Na+ 动作电位发放诱导的变化相比很小,这表明通过高电压激活的Ca2+ 通道的Ca2+ 内流是Na+ 动作电位相关[Ca2+]i增加的主要原因。3. 在以恒定频率(> 20 Hz)持续发放Na+ 动作电位期间,[Ca2+]i分别在树突中约1 s和胞体中约2 s后达到恒定水平。达到的水平幅度与发放频率呈正相关。我们认为,在紧张性活动期间,[Ca2+]i达到由Ca2+ 内流和外流决定的稳态。4. TTX抗性平台电位在树突中引起的[Ca2+]i增加比胞体中更大。在树突中,与平台相关的Ca2+ 瞬变在幅度上与由短(50 ms)Na+ 动作电位串触发的Ca2+ 瞬变相当,在胞体中则小得多。5. 与一阵Na+ 动作电位相关的低阈值尖峰(LTSs)在胞体和树突中均诱导[Ca2+]i急剧增加。(摘要截断于250字)

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