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体外培养的大鼠纹状体神经元中,再生性钙电位背后的内向钙电流被Bay K 8644增强。

An inward calcium current underlying regenerative calcium potentials in rat striatal neurons in vitro enhanced by Bay K 8644.

作者信息

Cherubini E, Lanfumey L

出版信息

Neuroscience. 1987 Jun;21(3):997-1005. doi: 10.1016/0306-4522(87)90054-6.

DOI:10.1016/0306-4522(87)90054-6
PMID:2442659
Abstract

The single electrode voltage clamp technique was used to characterize the currents underlying the calcium potentials in rat caudate neurons in vitro. In current clamp experiments, long depolarizing current pulses evoked repetitive firing of fast somatic action potentials. These were abolished by tetrodotoxin (1 microM) and replaced by slow graded depolarizing potentials. These were preceded by a transient hyperpolarizing notch. Addition of 4-aminopyridine (100 microM) abolished the hyperpolarizing notch, enhanced the slow graded depolarizing response and induced the appearance of a slow all-or-nothing action potential. Both the slow graded response and the all-or-nothing action potential were abolished by cobalt (2 mM), suggesting the involvement of voltage-dependent calcium conductances. When the neurons were loaded intracellularly with caesium the action potential duration increased. Substitution of the extracellular calcium by barium (1-3 mM) or external addition of tetraethylammonium (5 mM) further prolonged spike duration and induced the appearance of long-lasting plateau potentials. These were insensitive to tetrodotoxin and were reversibly blocked by the calcium antagonists cobalt (2 mM), manganese (2 mM) or cadmium (500 microM). The calcium potentials were enhanced by the calcium 'agonist' BAY K 8644 (1-5 microM). In voltage clamp experiments when intracellular caesium was used to reduce outward currents and tetrodotoxin to block fast regenerative sodium currents, depolarizing voltage steps from a holding potential of -50, -40 mV activated an inward current. This current peaked in 50-80 ms and inactivated in two phases: an initial one at 150-200 ms followed by a second one after several hundred ms.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

采用单电极电压钳技术对体外培养的大鼠尾状核神经元钙电位相关电流进行特性分析。在电流钳实验中,长时间的去极化电流脉冲诱发快速的体细胞动作电位重复发放。这些动作电位被河豚毒素(1微摩尔)阻断,并被缓慢的分级去极化电位所取代。在这些电位之前有一个短暂的超极化切迹。加入4-氨基吡啶(100微摩尔)可消除超极化切迹,增强缓慢的分级去极化反应,并诱导出现缓慢的全或无动作电位。缓慢的分级反应和全或无动作电位均被钴(2毫摩尔)阻断,提示电压依赖性钙电导参与其中。当神经元细胞内加载铯时,动作电位时程延长。用钡(1 - 3毫摩尔)替代细胞外钙或在细胞外加入四乙铵(5毫摩尔)可进一步延长动作电位时程,并诱导出现持久的平台电位。这些电位对河豚毒素不敏感,可被钙拮抗剂钴(2毫摩尔)、锰(2毫摩尔)或镉(500微摩尔)可逆性阻断。钙“激动剂”BAY K 8644(1 - 5微摩尔)可增强钙电位。在电压钳实验中,当细胞内使用铯减少外向电流,并用河豚毒素阻断快速再生性钠电流时,从 - 50、- 40毫伏的钳制电位进行去极化电压阶跃可激活内向电流。该电流在50 - 80毫秒达到峰值,并在两个阶段失活:最初在150 - 200毫秒,随后在几百毫秒后出现第二个阶段。(摘要截断于250字)

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