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논문 기본 정보

자료유형
학술저널
저자정보
Kim, Han-Seop (Department of Biological Science, College of Natural Sciences, Ajou University) Lee, Changho (Department of Pharmacology, College of Medicine, Hanyang University) Min, Churl K. (Department of Biological Science, College of Natural Sciences, Ajou University)
저널정보
한국통합생물학회 Korean journal of biological sciences Korean journal of biological sciences 제2권 제4호
발행연도
1998.1
수록면
471 - 476 (6page)

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The G protein-activated inwardly rectifying $K^+$ channel (GIRK1) was coex-pressed in Xenopus oocytes along with the $5-HT_{1A}$ receptor, a 7-helix receptor known to be coupled to $K^+$ channels in many neural tissues. Thus, the activation of the $5-HT_{1A}$ receptor by its agonist leads to the opening of GIRK1. The GIRK1 current was measured using the two electrode voltage clamp technique with bath application of 5-HT in the presence of various external potassium concentrations $[K^+]_0$. GIRK1 showed a strong inward rectification since only hyperpolarizing voltages evoked inward currents. $K^{+}$ was the major ion carrier as evidenced by about 44㎷ voltage shift corresponding to a 10-fold external 〔$K^+$〕 change. 5-HT induced a concentration-dependent inward $K^+$ current ($EC_{50}{\equation omitted}10.7nM$) which was blocked by $Ba^{2+}$. Pertussis toxin (PTX) pre-treatment reduced the $K^+$ current by as much as about 70%, suggesting that PTX-sensitive G protein ($G_i or G_o$ type) are involved in the $5-HT_{1A}$ receptor-GIRK1 coupling in Xenopus oocytes.

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