GABA_(B)受体对牛磺酸调节突触体氨基酸释放的影响

Effect of GABA_(B) receports on taurine-regulate release of amino acids from rat cortical synaptosomes

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。

AIM Taurine can regulate Asp、 Glu、 GABA from rat cortical synaptosomes. But its mechanism is unclear. The release regulated effects were investigated through analysis of GABA receptors.METHODS Bicuculline、Phaclofen、Baclofen were added in a Krebs Ringer buffer with resuspended synapotomes.Endogenous Asp、 Glu and GABA release during the 5 min superfusion were measured by high perfusion liquid chromatography using percolumn durivatization with Dans Cl. RESULT Phaclofen,but not bicucullion baclofen, counteracted the inhibition of GABA overflow,although the inhibition of Asp and Glu overflow was not attenuated. CONCLUSION Taurine inhibits the depolarization evoked release of GABA through the activation of presynaptic autoreceptors and taurine also acts on presynaptic sits of Asp Glu nerve terminals to inhibit their evoked release in rat cerebral cotex.