Regulation of glutamate neurotransmission by endogenous Zn^<++>

1. L-谷氨酸对Zn^<2+>结合蛋白的影响：我们在大鼠海马的胞浆部分发现了一种Zn^<2+>结合蛋白。L-谷氨酸及其类似物刺激Zn^2+从蛋白质上解离。在大鼠海马内长期应用锌离子螯合剂双硫腙可降低L-谷氨酸的水平，但对其他递质的水平无影响。2.蛋白激酶C（PKC）的转位：在海马突触神经体中，NMDA和L-谷氨酸可诱导PKC从胞浆转位至质膜。NMDA诱导的易位依赖于Ca^<2+>和微量的内源性Zn^<2+>。L-谷氨酸释放的调节：Zn^2+抑制海马脑片L-谷氨酸的释放，但不抑制GABA和乙酰胆碱的释放，而双硫腙增加L-谷氨酸的释放。Zn^<2+>可抑制NMDA对卡巴胆碱诱导的PI（phosphatidilinositol）转换的抑制作用，其作用机制可能与Zn^<2 +>抑制Ca^<2 +>内流有关。

1.Effect of L-glutamate on Zn^<2+> binding protein: We found a Zn^<2+> binding protein in cytosolic fraction of rat hippocampus. L-glutamate and its analogues stimulated the dissociation of Zn^<2+> form the protein. Chronic application of a Zn^<2+> chelator, dithizone, into rat hippocampus decreased the level of L-glutamate but not those of the other transmitters.2.Translocation of protein kinase C (PKC) : In hippocampla synaptoneurosome, NMDA and L-glutamate induced translocation of PKC from cytosol to plasma membrane. The NMDA-induced translocation was dependent on Ca^<2+> and required for trace amount of endogenous Zn^<2+>. The effect of NMDA showed a developmental changes, where the effect was most obvious at 7 day from the birth.3.Regulation of L-glutamate release: Zn^<2+> inhibited release of L-glutamate, but not those of GABA and acethycholine, from hippocampal slices, while dithizone increased the L-glutamate release.4.Inhibition of PI turnover: The inhibition of NMDA on carbachol-induced PI(phosphatidilinositol) turnover was suppressed by Zn^<2+> The effect was caused by inhibition of Ca^<2+> influx by Zn^<2+>.