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首页> 外文期刊>Brain research >Allosteric modulation of (3H)dizocilpine binding to N-methyl-D-aspartate receptor by an endogenous Na(+), K(+)-ATPase inhibitor: dependence on receptor activation.
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Allosteric modulation of (3H)dizocilpine binding to N-methyl-D-aspartate receptor by an endogenous Na(+), K(+)-ATPase inhibitor: dependence on receptor activation.

机译：（3H）dizocilpine的变构调制通过内源性Na（+），K（+）-ATPase抑制剂与N-甲基-D-天冬氨酸受体结合：依赖于受体激活。

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摘要

An endogenous Na(+), K(+)-ATPase inhibitor, termed endobain E, has been isolated from rat brain and proved to decrease [3H]dizocilpine binding to cerebral cortex N-methyl-D-aspartate (NMDA) receptor, an effect independent of sodium pump activity. The purpose of this study was to disclose the mechanism of [3H]dizocilpine binding reduction by endobain E by performing saturation, kinetic and competitive assays. In saturation binding assays, endobain E increased K(d) without modifying B(max) value. To determine whether competitive or allosteric interaction was involved, kinetics of [3H]dizocilpine binding to cerebral cortex membranes was studied. Endobain E increased [3H]dizocilpine dissociation rate constant and induced an initial fast phase, without modifying association rate constant, indicating an allosteric interaction. In competitive [3H]dizocilpine binding assays, no additive effect was observed with endobain E plus competitive antagonists for glutamate or glycine sites (2-amino-5-phosphonopentanoicacid (AP-5) and 7-chlorokynurenic acid, respectively), indicating that coagonist site blockade interferes with endobain E effect. However, the higher glutamate and glycine concentration, the greater its effect. Endobain E binding reduction was partially additive with that induced by ketamine or Mg(2+) (receptor-associated channel blockers). Results suggest that the greater the channel activation by glutamate and glycine, the greater endobain E allosteric effect. Furthermore, as ketamine and Mg(2+) interfere with endobain E effect, this factor most likely binds to the inner surface of the NMDA associated channel.
机译：已从大鼠大脑中分离出一种内源性Na（+），K（+）-ATPase抑制剂，称为内啡肽E，已证明可降低[3H] dizocilpine与脑皮质N-甲基-D-天冬氨酸（NMDA）受体的结合。作用与钠泵活动无关。这项研究的目的是通过进行饱和，动力学和竞争性分析来揭示内啡肽E降低[3H]二唑西平结合的机理。在饱和结合试验中，内皮糖蛋白E增加了K（d）而没有改变B（max）值。为了确定是否涉及竞争相互作用或变构相互作用，研究了[3H]二唑西平与大脑皮层膜结合的动力学。 Endobain E增加了[3H] dizocilpine的解离速率常数，并诱导了一个初始的快速期，而没有改变缔合速率常数，这表明变构相互作用。在竞争性[3H]双唑西平结合试验中，内皮糖蛋白E加上竞争性拮抗剂对谷氨酸或甘氨酸位点（分别为2-氨基-5-膦基戊酸（AP-5）和7-氯尿嘧啶酸）未观察到累加作用，表明该拮抗剂部位封锁会干扰内皮糖蛋白E的作用。但是，谷氨酸和甘氨酸浓度越高，其作用越大。 Endobain E结合减少与氯胺酮或Mg（2 +）（受体相关通道阻滞剂）诱导的结合减少。结果表明，谷氨酸和甘氨酸对通道的激活作用越大，内皮素E的变构作用越大。此外，由于氯胺酮和Mg（2+）会干扰内皮素E的作用，该因子很可能与NMDA相关通道的内表面结合。

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