위 평활근에서 아세틸콜린의 저분극 기전에 관한 연구
Background/Aims: Acetylcholine which is a major excitatory neurotransmitter, depolarizes gastric smooth muscle cells. The aim of this study was to investigate the ionic mechanisms of acetylcholine-induced depolarization in antral myocytes of guinea-pig. Methods: Gastric myocytes were isolated from t...
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Published in: | The Korean journal of gastroenterology Vol. 31; no. 4; pp. 421 - 431 |
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Main Authors: | , , , , , , , , , , , , , |
Format: | Journal Article |
Language: | Korean |
Published: |
대한소화기학회
01-01-1998
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Subjects: | |
Online Access: | Get full text |
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Summary: | Background/Aims: Acetylcholine which is a major excitatory neurotransmitter, depolarizes gastric smooth muscle cells. The aim of this study was to investigate the ionic mechanisms of acetylcholine-induced depolarization in antral myocytes of guinea-pig. Methods: Gastric myocytes were isolated from the antral circular layer of guinea-pig using a collagenase. Then, we recorded membrane currents using the whole-cell patch clamp method. Results: Acetylcholine suppressed Ca2+- dependent K+ currents, whereas delayed rectifier K+ currents and voltage dependent Ca2+ currents were not changed. Under voltage clamp at -50 mV, acetylcholine activated inward currents. It was characterized by voltage-dependent and Ca2+-dependent cationic current. In the high concentration of extracellular K+ (90 mM), lemakalim produced inward currents, which could be blocked by glibenclamide, a specific blocker of ATP-sensitive K+ channel. Acetylcholine suppressed these glibenclamide-sensitive K+ currents. Conclusions: The results of this study suggested that the depolarizing mechanism of acetylcholine might be caused from the combined effects of the suppression of Ca2+-dependent K+ currents, the activation of non-specific cationic current and the suppression of glibenclamide-sensitive K+ currents. (Korean J Gastroenterol 1998;31:421 - 431) |
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Bibliography: | Korean Society of Gastroenterology |
ISSN: | 1598-9992 |