Neuropharmacological study on excitatory amino acid receptors in hippocampus

1. 兴奋性氨基酸受体结合：谷氨酸（glu）半胱氨酸亚磺酸，兴奋性氨基酸激动剂，在大鼠突触膜上有不同的结合位点。cl依赖的葡聚糖结合位点与cl依赖的葡聚糖分离有关。脑切片的去极化伴随着glu的cl依赖性结合位点的特异性增加。此外，半胱酸，一种兴奋性硫氨基酸，是这种cl依赖的葡氨酸结合位点的特异性配体。海马切片中环状AMP的形成：兴奋性氨基酸。如谷氨酸和亚磺酸半胱氨酸，通过其自身在海马中的受体显著促进环AMP的形成。完全依赖于Cl离子表明Cl转运是兴奋性氨基酸受体介导的环AMP形成的刺激所必需的。氨基酸神经递质释放：兴奋性氨基酸增强GAGA释放是由兴奋性氨基酸受体介导的。胰岛素和锌离子特异性地减弱亚硫酸半胱氨酸对GABA释放的刺激作用。此外，锌离子特异性地抑制了预负荷海马切片中谷氨酸的释放。锌离子以蛋白聚集体形式存在于海马可溶部分。兴奋性氨基酸，尤其是准质氨基酸，刺激结合蛋白释放Zn离子。

1. Excitatory amino acid receptor binding:Glutamate (glu) cysteine sulfinate, excitatory amino acid agonists, have different binding sites in synaptic membranes of rat. Cl-Dependent glu binding sites are related,to Cl-dependent sequestration of glu. Depolarization of brain slices are accompanied by a specific increase in the Cl-dependent binding sites for glu. Furthemore, cysteic acid, an excitatory sulfur amino acid, is a specific ligand for this Cl-dependent glu binding site.2. Cyclic AMP formation in hippocampal slices:Excitatory amino acids. such as glu and cysteine sulfinate, markedly enhance the formation of cyclic AMP through their own receptors in hippocampus. Complete dependency on Cl ion indicates that Cl transport is essential for excitatory amino acid receptors-mediated stimulation of cyclic AMP formation.3. Release of amino acid neurotransmitter:Enhancement of GAGA release by excitatory amino acids is mediated by excitatory amino acid receptors. Insulim and Zn ion specifically attenuated the stimulatory effect of cysteine sulfinate on GABA release. In addition, Zn ion specifically inhibited the release of glu from the preloaded hippocampal slices. Zn ion localized in the soluble fraction of hippocampus as proteinbound form. Excitatory amino acids, especially quisqualate, stimulated the release of Zn ion from the binding proteins.