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强直刺激后鸡睫状神经节杯状神经末梢中的钙浓度变化

Calcium concentration changes in the calyciform nerve terminal of the avian ciliary ganglion after tetanic stimulation.

作者信息

Larkum M E, Warren D A, Bennett M R

机构信息

Department of Physiology, University of Sydney, NSW, Australia.

出版信息

J Auton Nerv Syst. 1994 Mar;46(3):175-88. doi: 10.1016/0165-1838(94)90035-3.

Abstract

A study has been made of the changes in calcium concentration in the calyciform nerve terminal ([Ca]c) and in the neurone soma ([Ca]s) of avian ciliary ganglion cells following tetanic stimulation of the nerve terminal. Dissociated ciliary neurones were loaded with the calcium indicator Fura-2 and digital imaging techniques used to determine the spatial and temporal distribution of calcium in the cells during post-tetanic potentiation (PTP) and long-term potentiation (LTP). Stimulation of the calyciform terminal with an extracellular electrode at 10 Hz for 2 s increased both [Ca]s and [Ca]s over 3-fold, with the [Ca] increasing for each impulse in the facilitatory train. The increase in [Ca]s could be prevented by allowing the terminal to degenerate in culture before stimulation. Stimulation of the calyciform terminal with a long tetanus of 30 Hz for 20 s gave an over 4-fold increase in both [Ca]c and [Ca]s by the end of the train. Analysis of the decline in [Ca]c after the train showed that it disappeared from the calyx along a double exponential time course with time constants of about 1 min and 50 min, respectively. These times are similar to those of PTP and LTP in the ganglia, and are almost independent of the extracellular calcium level. In order to determine whether the influx of calcium ions during a tetanus was through N-type calcium channels, these were blocked with adenosine (100 microM). Adenosine blocked the increase in both [Ca]s and [Ca]c that normally accompanies a tetanus. Thapsigargin (200 nM) did not affect [Ca]c or [Ca]s, but blocked transient increases in [Ca] caused by caffeine (10 mM) in both 3 mM and Ca2+ free bath solutions. These results are discussed in relation to the role of intracellular calcium in initiating LTP after a tetanus to the nerve terminals.

摘要

一项研究对神经末梢强直刺激后鸡睫状神经节细胞的杯状神经末梢钙浓度([Ca]c)和神经元胞体钙浓度([Ca]s)的变化进行了研究。分离的睫状神经元用钙指示剂Fura-2进行负载,并使用数字成像技术来确定强直后增强(PTP)和长时程增强(LTP)期间细胞内钙的时空分布。用细胞外电极以10 Hz刺激杯状末梢2 s,使[Ca]s和[Ca]c均增加了3倍以上,在易化串中的每个冲动时[Ca]c都会增加。通过在刺激前让末梢在培养中退化,可以防止[Ca]s的增加。用30 Hz的长时强直刺激杯状末梢20 s,在刺激结束时[Ca]c和[Ca]s均增加了4倍以上。对刺激后[Ca]c下降的分析表明,它从杯状结构中以双指数时间进程消失,时间常数分别约为1分钟和50分钟。这些时间与神经节中PTP和LTP的时间相似,并且几乎与细胞外钙水平无关。为了确定强直期间钙离子的内流是否通过N型钙通道,用腺苷(100 microM)将其阻断。腺苷阻断了通常伴随强直出现的[Ca]s和[Ca]c的增加。毒胡萝卜素(200 nM)不影响[Ca]c或[Ca]s,但在3 mM和无Ca2+的浴液中均阻断了咖啡因(10 mM)引起的[Ca]的瞬时增加。结合细胞内钙在神经末梢强直后引发LTP中的作用对这些结果进行了讨论。

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