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视网膜双极神经元中的钙动作电位。

Calcium action potentials in retinal bipolar neurons.

作者信息

Zenisek D, Matthews G

机构信息

Department of Neurobiology and Behavior, State University of New York, Stony Brook 11794-5230, USA.

出版信息

Vis Neurosci. 1998 Jan-Feb;15(1):69-75. doi: 10.1017/s0952523898151064.

DOI:10.1017/s0952523898151064
PMID:9456506
Abstract

Patch-clamp and calcium-indicator measurements were used to examine the electrical excitability of large-terminal bipolar neurons from goldfish retina. Large, transient increases in intracellular calcium occurred spontaneously in the synaptic terminal but not in the soma of bipolar neurons. Calcium transients were blocked by hyperpolarization, by external application of calcium-channel blockers, and by the neurotransmitters GABA and glutamate. These observations suggest that calcium action potentials are responsible for the spontaneous increases in intraterminal calcium, which was directly confirmed by electrical recordings of calcium-dependent action potentials in both whole-cell and perforated-patch recordings. We suggest that regenerative depolarization produced by the opening of calcium channels in the synaptic terminal of on-type bipolar neurons represents an amplification mechanism in the high-sensitivity ON pathway in the dark-adapted fish retina.

摘要

采用膜片钳和钙指示剂测量法来检测金鱼视网膜大终末双极神经元的电兴奋性。双极神经元的突触终末会自发出现大幅度、瞬时性的细胞内钙增加,但胞体中不会出现这种情况。超极化、细胞外应用钙通道阻滞剂以及神经递质γ-氨基丁酸(GABA)和谷氨酸可阻断钙瞬变。这些观察结果表明,钙动作电位是终末内钙自发增加的原因,全细胞记录和穿孔膜片钳记录中对钙依赖性动作电位的电记录直接证实了这一点。我们认为,在暗适应的鱼类视网膜中,ON型双极神经元突触终末钙通道开放产生的再生性去极化代表了高灵敏度ON通路中的一种放大机制。

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