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豚鼠嗜铬细胞中的毒蕈碱受体激活会导致膜电导降低和去极化。

Muscarinic receptor activation in guinea-pig chromaffin cells causes decreased membrane conductance and depolarization.

作者信息

Holman M E, Tonta M A, Coleman H A, Parkington H C

机构信息

Department of Physiology, Monash University, Clayton, Vic., Australia.

出版信息

J Auton Nerv Syst. 1998 Feb 5;68(3):140-4. doi: 10.1016/s0165-1838(97)00122-7.

Abstract

Membrane potentials were recorded with conventional intracellular microelectrodes from chromaffin cells in isolated, bisected adrenal glands from guinea-pigs. The local pressure ejection of muscarinic agonists, acetylcholine (in the presence of hexamethonium) or bethanecol, caused a transient depolarization that was relatively slow (1-2 s) in onset compared with the depolarization associated with the activation of nicotinic receptors. Muscarinic receptor-induced depolarization was associated with an increase in input resistance and the firing of action potentials. Repetitive stimulation of splanchnic nerve fibers within the gland, in the presence of hexamethonium, caused a maintained depolarization that was slow in both onset and decay and in many cells caused the repetitive firing of action potentials. It is suggested that, in this species, the exocytosis of catecholamines caused by the activation of muscarinic receptors, described by others, may be due to the initiation of tetrodotoxin-sensitive action potentials and consequent opening of voltage sensitive Ca2+ channels.

摘要

使用传统的细胞内微电极,从豚鼠分离的、二分的肾上腺嗜铬细胞中记录膜电位。在六甲铵存在的情况下,毒蕈碱激动剂乙酰胆碱或氨甲酰甲胆碱的局部压力喷射会引起短暂的去极化,与烟碱样受体激活相关的去极化相比,其起始相对较慢(1-2秒)。毒蕈碱受体诱导的去极化与输入电阻增加和动作电位发放有关。在六甲铵存在的情况下,对腺体内的内脏神经纤维进行重复刺激会导致持续的去极化,其起始和衰减都很缓慢,并且在许多细胞中会导致动作电位的重复发放。有人提出,在这个物种中,其他人描述的由毒蕈碱受体激活引起的儿茶酚胺胞吐作用,可能是由于河豚毒素敏感的动作电位的启动以及随后电压敏感Ca2+通道的开放。

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