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

1.l -谷氨酸对Zn^<2+>结合蛋白的影响：我们在大鼠海马细胞质部分发现了Zn^<2+>结合蛋白。l -谷氨酸及其类似物刺激Zn^<2+>从蛋白质中解离。大鼠海马长期应用Zn^<2+>螯合剂双硫腙可降低l -谷氨酸水平，但对其他递质无明显影响。蛋白激酶C （PKC）易位：在海马突触eurosome中，NMDA和l -谷氨酸诱导PKC从细胞质溶胶向质膜易位。nmda诱导的易位依赖于Ca^<2+>，需要微量的内源Zn^<2+>。NMDA的作用表现为发育变化，在出生后第7天效果最明显。3 .对l -谷氨酸释放的调节：Zn^<2+>能抑制海马片中l -谷氨酸的释放，但对GABA和乙酰胆碱的释放无抑制作用，而双硫腙能增加l -谷氨酸的释放。抑制PI周转：NMDA对碳甾醇诱导的PI（磷脂酰肌醇）周转的抑制作用是由Zn^<2+>抑制Zn^<2+>抑制Ca^<2+>内流所致。

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+>.