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体外培养的大鼠海马神经元在短暂一串动作电位后早期超极化后电位的特征

Characterization of an early afterhyperpolarization after a brief train of action potentials in rat hippocampal neurons in vitro.

作者信息

Williamson A, Alger B E

机构信息

Department of Physiology, University of Maryland School of Medicine, Baltimore 21201.

出版信息

J Neurophysiol. 1990 Jan;63(1):72-81. doi: 10.1152/jn.1990.63.1.72.

DOI:10.1152/jn.1990.63.1.72
PMID:2299387
Abstract
  1. In rat hippocampal pyramidal cells in vitro, a brief train of action potentials elicited by direct depolarizing current pulses injected through an intracellular recording electrode is followed by a medium-duration afterhyperpolarization (mAHP) and a longer, slow AHP. We studied the mAHP with the use of current-clamp techniques in the presence of dibutyryl cyclic adenosine 3',5'-monophosphate (cAMP) to block the slow AHP and isolate the mAHP. 2. The mAHP evoked at hyperpolarized membrane potentials was complicated by a potential generated by the anomalous rectifier current, IQ. The mAHP is insensitive to chloride ions (Cl-), whereas it is sensitive to the extracellular potassium concentration ([K+]o). 3. At slightly depolarized levels, the mAHP is partially Ca2+ dependent, being enhanced by increased [Ca2+]o and BAY K 8644 and depressed by decreased [Ca2+]o, nifedipine, and Cd2+. The Ca2(+)-dependent component of the mAHP was also reduced by 100 microM tetraethylammonium (TEA) and charybdotoxin (CTX), suggesting it is mediated by the voltage- and Ca2(+)-dependent K+ current, IC. 4. Most of the Ca2(+)-independent mAHP was blocked by carbachol, implying that IM plays a major role. In a few cells, a small Ca2(+)- and carbachol-insensitive mAHP component was detectable, and this component was blocked by 10 mM TEA, suggesting it was mediated by the delayed rectifier current, IK. The K+ channel antagonist 4-aminopyridine (4-AP, 500 microM) did not reduce the mAHP. 5. We infer that the mAHP is a complex potential due either to IQ or to the combined effects of IM and IC. The contributions of each current depend on the recording conditions, with IC playing a role when the cells are activated from depolarized potentials and IM dominating at the usual resting potential. IQ is principally responsible for the mAHP recorded at hyperpolarized membrane potentials.
摘要
  1. 在体外培养的大鼠海马锥体细胞中,通过细胞内记录电极注入的直接去极化电流脉冲引发的一串短暂动作电位之后,会出现一个中等时长的超极化后电位(mAHP)和一个更长的慢超极化后电位。我们在存在二丁酰环磷腺苷(cAMP)以阻断慢超极化后电位并分离出mAHP的情况下,使用电流钳技术研究了mAHP。2. 在超极化膜电位下诱发的mAHP因反常整流电流IQ产生的电位而变得复杂。mAHP对氯离子(Cl-)不敏感,而对细胞外钾离子浓度([K+]o)敏感。3. 在轻度去极化水平时,mAHP部分依赖于Ca2+,细胞外Ca2+浓度([Ca2+]o)升高和BAY K 8644可增强它,而[Ca2+]o降低、硝苯地平和Cd2+可抑制它。mAHP的Ca2+依赖成分也被100微摩尔四乙铵(TEA)和蝎毒素(CTX)降低,这表明它是由电压和Ca2+依赖的钾电流IC介导的。4. 大部分不依赖Ca2+的mAHP被卡巴胆碱阻断,这意味着IM起主要作用。在少数细胞中,可检测到一个小的对Ca2+和卡巴胆碱不敏感的mAHP成分,该成分被10毫摩尔TEA阻断,表明它是由延迟整流电流IK介导的。钾通道拮抗剂4-氨基吡啶(4-AP,500微摩尔)并未降低mAHP。5. 我们推断,mAHP是一个复杂电位,要么归因于IQ,要么归因于IM和IC的联合作用。每种电流的贡献取决于记录条件,当细胞从去极化电位激活时IC起作用,而在通常的静息电位时IM占主导。IQ主要负责在超极化膜电位记录到的mAHP。

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