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首页> 美国卫生研究院文献>The Journal of Neuroscience >Induction of glutamate binding sites in hippocampal membranes by transient exposure to high concentrations of glutamate or glutamate analogs
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Induction of glutamate binding sites in hippocampal membranes by transient exposure to high concentrations of glutamate or glutamate analogs

机译：通过短暂暴露于高浓度的谷氨酸盐或谷氨酸盐类似物诱导海马膜中的谷氨酸盐结合位点

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摘要

The number of Na+-independent, Cl--dependent glutamate binding sites in rat hippocampal membranes is increased two- to fourfold after pre- exposing isolated membranes or hippocampal slices to high concentrations (0.1–10 mM) of L-glutamate or of glutamate analogs with high affinity for this binding site, such as quisqualate, homocysteate, or aminoadipate. N-Methylaspartate and kainate are ineffective. A similar binding increase is induced by transient exposure to the dipeptide tyrosylglutamate. The newly induced binding sites appear to be identical with pre-existing Cl--dependent binding sites by several criteria: They have a similar pharmacological profile, they are sensitive to low concentrations of Na+, and the number of sites can be further increased by transient exposure to micromolar calcium concentrations. Moreover, binding of [3H]APB, a ligand selective for the Cl--dependent glutamate binding sites, is also increased after glutamate preincubation. The induction of binding sites by high glutamate concentrations, described herein, is calcium-independent, not inhibited by leupeptin and, therefore, different from the previously described activation of binding sites by a calcium-sensitive protease. The high concentration of ligand needed to induce increased binding suggests the presence in hippocampal membranes of a binding site with low, millimolar affinity that is functionally related to the known high- affinity binding sites. Several interpretations of the observed effects and their implications for the possible relationship between the binding site and the synaptic receptor are discussed.
机译：将分离的膜或海马切片暴露于高浓度（0.1–10 mM）的L-谷氨酸或谷氨酸类似物后，大鼠海马膜中Na +依赖性，Cl依赖性谷氨酸结合位点的数目增加了2-4倍。对这个结合位点具有高亲和力，例如准喹啉，高半胱氨酸或氨基己二酸。 N-天冬氨酸甲酯和海藻酸酯无效。瞬时暴露于二肽酪氨酰谷氨酸盐可诱导类似的结合增加。通过几个标准，新诱导的结合位点似乎与先前存在的Cl依赖性结合位点相同：它们具有相似的药理学特征，对低浓度的Na +敏感，并且瞬时增加可进一步增加位点数量暴露于微摩尔钙浓度。此外，在谷氨酸预孵育后，[3H] APB（一种对依赖Cl的谷氨酸结合位点有选择性的配体）的结合也增加了。本文所述的通过高谷氨酸浓度诱导结合位点是钙依赖性的，不受亮肽素抑制，因此，与先前描述的钙敏感蛋白酶对结合位点的激活不同。诱导增加的结合所需的高浓度配体表明在海马膜中存在具有与已知的高亲和力结合位点功能相关的低，毫摩尔亲和力的结合位点。讨论了观察到的效果的几种解释及其对结合位点和突触受体之间可能关系的暗示。

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