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目的研究γ-氨基丁酸(GABA)受体对离子型谷氨酸受体的调控机制。方法采用细胞膜片钳电生理技术,以GABA、谷氨酸(Glu)刺激记录GABA受体及Glu受体离子通道介导的全细胞电流(IGABA,IGlu),观察GABA对谷氨酸受体离子通道活性的调控;并以荷包牡丹碱(Bic)抑制IGABA、以SO24-或葡萄糖酸根(gluconate-)代替Cl-,研究其抑制作用的分子机制。结果相同浓度GABA与Glu共给药诱导IGABA+Glu较单独给药诱导电流IGABA与IGlu之和小,该差异随浓度升高而降低;不同浓度GABA对Glu30μmol/L诱导电流IGlu抑制作用随GABA浓度升高而增强,该抑制作用可以被Bic、SO24-与gluconate-消除。结论 GABAA受体能抑制谷氨酸受体介导的全细胞电流,该作用具有浓度依赖性,其抑制机制可能与Cl-的通透性有关。
Aim To study the regulatory mechanism of γ-aminobutyric acid (GABA) receptors on ionotropic glutamate receptors. Methods Cell-patch-clamp electrophysiological techniques were used to record GABA and Glu receptor ion channel-mediated global cell currents (IGABA and IGlu) by GABA and Glu. The effect of GABA on glutamate receptor ion Channel activity. The inhibitory effects of bicuculline (Bic) on IGABA and SO24- or gluconate- on Cl- were also investigated. Results Compared with single administration of GABA and Glu, the same dose of IGABA plus Glu resulted in a smaller sum of IGABA and IGlu, which was decreased with increasing concentration of GABA. The effect of different concentrations of GABA on Glulucose induced apoptosis was similar to that of GABA Increased and enhanced, the inhibition can be Bic, SO24- and gluconate-elimination. Conclusion GABAA receptor can inhibit glutamate receptor-mediated whole cell currents in a concentration-dependent manner, and its inhibitory mechanism may be related to the permeability of Cl-.