Present study was performed to clarify the effect of acetylcholine on the release of gamma-aminobutyric acid(GABA) employing hippocampal slices. Hippocampal slices (300∼400㎛ thick) were prepared by the method of Kim et al(1988) and pre-equilibrat...
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https://www.riss.kr/link?id=A19562329
1991
Korean
515.000
KCI등재후보
학술저널
104-110(7쪽)
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
Present study was performed to clarify the effect of acetylcholine on the release of gamma-aminobutyric acid(GABA) employing hippocampal slices. Hippocampal slices (300∼400㎛ thick) were prepared by the method of Kim et al(1988) and pre-equilibrat...
Present study was performed to clarify the effect of acetylcholine on the release of gamma-aminobutyric acid(GABA) employing hippocampal slices.
Hippocampal slices (300∼400㎛ thick) were prepared by the method of Kim et al(1988) and pre-equilibrated in Krebs-bicarbonate medium(KBM, pH 7.4) for 1hr at 37℃. Pre-equilibrated slices were incubated in fresh KBM and then potassium(50mM)-containing KBM for 5 min period. Basal and potassium-induced release of GABA were determined from recovered medium by HPLC. After 30min resting period, in the presence of physostigmine(20μM) slices were reincubated in acetylcholine-containing KBM and acetylcholine plus potassium-containing medium consecutively for 5min period each to investigate the effect of acetylcholine on basal or potassium-induced GABA release from hippocampal slices.
The observed results were as follows:
1. The release of GABA induced by the first and second 5 min-exposure of 50mM potassium was 107.3±8.2 nmol and 90.6±3.2nmol, respectively. When compared with released amounts of GABA during the corresponding spontaneous periods, these were 4.6 and 4.6-fold increase respectively.
2. Physostigmine(20μM) had no significant effect on the spontaneous release of GABA.
3. Acetylcholine(10-1000μM) increased spontaneous and potassium-induced GABA release in a dose-dependent manner.
방사선 멸균된 냉동건조 동종골의 재소독 효과에 관한 연구
Effect of adrenergic agonists on Na^+ -K^+ -ATPase activity of rat parotid acinar cells