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目的 牛磺酸 (Tau)调节大鼠大脑皮层突触体Asp、Glu、GABA的释放的机制尚不清楚 ,本研究从GABA受体的角度进行探讨。方法 将 phaclofen、biculline、baclofen加入悬浮有突触体的KRB液中 ,氨基酸测定采用Dans Cl柱前衍生 ,高效液相测定。结果 Tau对GABA释放的抑制作用能有效被Phaclofen所拮抗 ,而它们对GluAsp的释放均无影响。结论 Tau抑制去极化引发GABA的释放是通过激发突触体前膜GABAB 受体而起作用的 ,同时还作用于Asp、Glu神经末梢的突触体前膜 ,从而抑制去极化引发的Asp、Glu的释放。
Purpose The mechanism of taurine (Tau) regulating the release of Asp, Glu and GABA in rat cerebral cortex synaptosomes is not yet clear. In this study, we investigated the mechanism of Tau release from GABA receptor. Methods Phaclofen, biculline and baclofen were added to the synaptosome-suspended KRB solution. The amino acids were determined by Dans Cl pre-column derivatization and HPLC. Results The inhibitory effect of Tau on GABA release was effectively antagonized by Phaclofen, and they had no effect on the release of GluAsp. Conclusions The Tau-induced depolarization-initiated GABA release acts by activating the GABAB receptor on the presynaptic membrane of the synaptosome and also acts on the presynaptic membrane of the presynaptic Asp and Glu nerve terminals to inhibit depolarization-induced Asp Glu release.