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钙与神经元可塑性。

Calcium and neuronal plasticity.

作者信息

Segal M

机构信息

Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.

出版信息

Isr J Med Sci. 1993 Sep;29(9):543-8.

PMID:8225943
Abstract

The proposed involvement of free intracellular calcium concentration ([Ca]i) in neuronal plasticity is examined. While it is generally believed that a rise of [Ca]i is necessary for the triggering of long-term modification of synaptic connections, there are many unresolved issues related to this dogma; it is not entirely clear what is the source of the elevated calcium, how much of a calcium rise is sufficient to produce the synaptic potentiation, where and for how long, and what are the relevant chemical consequences of the transient rise of [Ca]i. It is generally believed that the dendritic spine is the locus of synaptic modification, yet little evidence exists to support this view. High resolution calcium imaging studies may contribute to the clarification of some key issues in the field of neuronal plasticity.

摘要

本文探讨了细胞内游离钙浓度([Ca]i)在神经元可塑性中的潜在作用。虽然人们普遍认为,[Ca]i升高对于触发突触连接的长期改变是必要的,但与这一信条相关的许多问题仍未得到解决;目前尚不完全清楚钙升高的来源是什么,钙升高多少足以产生突触增强,在何处以及持续多长时间,以及[Ca]i瞬时升高的相关化学后果是什么。人们普遍认为树突棘是突触修饰的位点,但几乎没有证据支持这一观点。高分辨率钙成像研究可能有助于阐明神经元可塑性领域中的一些关键问题。

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Glycine-activated currents are changed by coincident membrane depolarization in developing rat auditory brainstem neurones.在发育中的大鼠听觉脑干神经元中,甘氨酸激活电流会因同时发生的膜去极化而改变。
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