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小脑浦肯野细胞中的成像电压和突触激活的钠瞬变

Imaging voltage and synaptically activated sodium transients in cerebellar Purkinje cells.

作者信息

Lasser-Ross N, Ross W N

机构信息

Department of Physiology, New York Medical College, Valhalla 10595.

出版信息

Proc Biol Sci. 1992 Jan 22;247(1318):35-9. doi: 10.1098/rspb.1992.0006.

Abstract

Transient changes in sodium concentration in response to electrical activity were detected in Purkinje cells by using the fluorescent indicator SBFI (Minta & Tsien (J. biol. Chem. 264, 19,449 (1989)). Fast sodium action potentials caused large increases in internal sodium concentration, [Na]i, in the soma and axon, and were generally undetectable in the dendrites. No changes were detected in the dendrites corresponding to calcium action potentials. The spatial distribution of these transients corresponds to that expected if the increase in [Na]i were the result of Na+ entry through voltage-dependent Na channels generating sodium spikes in the axon hillock and soma. The [Na]i transients rapidly recovered (tau less than 1 s) in the axon hillock, probably by Na+ diffusion into the soma. Climbing fibre activation produced distinct [Na]i transients in the dendrites in addition to somatic and axonal signals. As regenerative potentials did not produce transients in this region, these signals may be caused by Na+ entry through ligand-gated channels. These results confirm and extend the description of channel distribution and electrical signalling in Purkinje cells.

摘要

通过使用荧光指示剂SBFI(明塔和钱永健(《生物化学杂志》264卷,第19449页(1989年))),在浦肯野细胞中检测到了钠浓度对电活动的瞬态变化。快速钠动作电位导致胞体和轴突内的钠浓度[Na]i大幅增加,而在树突中通常检测不到。与钙动作电位相对应的树突中未检测到变化。这些瞬态的空间分布与预期相符,即如果[Na]i的增加是由于Na+通过电压依赖性Na通道进入,从而在轴丘和胞体中产生钠尖峰的结果。轴丘中的[Na]i瞬态迅速恢复(时间常数小于1秒),可能是由于Na+扩散到胞体中。攀缘纤维激活除了产生胞体和轴突信号外,还在树突中产生明显的[Na]i瞬态。由于再生电位在该区域未产生瞬态,这些信号可能是由Na+通过配体门控通道进入引起的。这些结果证实并扩展了对浦肯野细胞中通道分布和电信号的描述。

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