小鼠胃中GABA摄取系统的负反馈式自身调节机制

A POSSIBLE MECHANISM FOR NEGATIVE FEEDBACK AUTOREGULATION OF GABA UPTAKE SYSTEM IN MOUSE STOMACH

应用同位素示踪法，研究了盐酸、胃蛋白酶、阿托品、蝇蕈醇和β－氯苯氨丁酸对离体培育的小鼠胃切片３Ｈ－ＧＡＢＡ摄取的影响。结果表明、盐酸（０．０１～０．６５Ｎ）、胃蛋白酶（０．０５～０．１ｍｇ／ｍｌ）均能显著地促进胃切片３Ｈ－ＧＡＢＡ摄取：而阿托品（０．０１～０．２５ｍｇ／ｍｌ）使摄取率显著减少。蝇蕈醇（０．５μｇ／ｍｌ）、β－氯苯氨丁酸（０．２～０．８ｍｇ／ｍｌ）也能显著促进胃切片３Ｈ－ＧＡＢＡ摄取。但是，阿托品预处理使蝇蕈醇和β－氯苯氨丁酸促进胃切片３Ｈ－ＧＡＢＡ摄取的效应完全消失。本研究结果提示，胃中可能存在一种ＧＡＢＡ摄取系统的负反馈式的自身调节机制。当胃酸、胃蛋白酶的分泌增强时，可促进ＧＡＢＡ摄取，使胃功能活动减弱，反之，当胃生理功能减弱时，则ＧＡＢＡ摄取受抑制，从而使胃功能活动增强。

The paper describes the effects of HCI, pepsin, atropin, muscimol and baclofen on GABA uptake of the mouse stomach slices by means of radio tracing in vitro. The results show that HCI (0.01～0.05N) and pepsin (0.05～0.1mg/ml) significantly accelerate the 3H-GABA uptake of stomach slices, whereas atropin (0.01～0.25 mg/ml) markedly decreases the 3H-GABA uptake rate of stomach slices. Muscimol (0.5μg/ml) and baclofen (0.2～0.8 mg/ml) also significantly accelerate the 3H-GABA uptake. The pretreatment of atropine can completely abolish the acceleration of muscimol and baclofen on the GABA uptake of stomach slices. The results suggest that possibly there is a mechanism of negative feedback autoregulation of GABA uptake system in mouse stomach. When the stomach functions mediated by GABA (for example, HCI and pepsin secretion) are strengthened, the GABA uptake in stomach will be increased and the physiological functions of stomach will be inhibited, thereby the functional activities of stomach will be maintained at a certain stable status.