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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Characterization of cyclothiazide-enhanced kainate excitotoxicity in rat hippocampal cultures.
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Characterization of cyclothiazide-enhanced kainate excitotoxicity in rat hippocampal cultures.

机译：大鼠海马培养物中环噻嗪增强的海藻酸酯兴奋性毒性的表征。

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Cyclothiazide has been shown to block desensitization of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)-preferring receptors and to enhance quisqualate-, AMPA- and kainate-induced neurotoxicity. The pharmacology behind this cyclothiazide-enhanced kainate-induced excitotoxicity was characterized in embryonic rat hippocampal cell cultures. Treatment of cell cultures with a combination of cyclothiazide and kainate for 24 h resulted in excessive neuronal death as measured by the release of lactate dehydrogenase into the culture media. Cyclothiazide produced a leftward shift of the kainate dose-response curve and enhanced the maximum response of kainate excitotoxicity. AMPA-preferring receptor antagonists, 2,3-dihydroxy-6-nitro-7-sulphamoyl-benzo(F)quinoxaline(NBQX) and 1-(4-amino-phenyl)-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine (GYKI 52466) blocked cyclothiazide-enhanced kainate toxicity completely, and cyclothiazide increased the IC50S for NBQX and GYKI 52466 against kainate toxicity. The N-methyl-D-aspartate (NMDA) antagonist, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine (MK801) also blocked cyclothiazide-enhanced kainate toxicity, but only partially. Cyclothiazide also increased the IC50 for MK801 against kainate toxicity. These data suggest that cyclothiazide enhances both AMPA-preferring receptor- and NMDA receptor-mediated toxicity in kainate-induced toxicity in embryonic rat hippocampal cultures.
机译：环丙沙胺已显示出可阻止α-氨基-3-羟基-5-甲基-5-甲基-4-异恶唑丙酸（AMPA）优先受体的脱敏作用，并增强喹喹啉，AMPA和海藻酸盐诱导的神经毒性。这种环噻嗪增强的海藻酸盐增强的兴奋性毒性背后的药理作用在胚胎大鼠海马细胞培养物中得到了表征。用环噻嗪和海藻酸盐的组合处理细胞培养物24小时会导致神经元过度死亡，这可以通过乳酸脱氢酶释放到培养基中来衡量。环乙肼会使海藻酸盐剂量反应曲线向左移动，并增强了海藻酸盐兴奋性毒性的最大反应。首选AMPA受体拮抗剂，2,3-二羟基-6-硝基-7-磺酰基-苯并（F）喹喔啉（NBQX）和1-（4-氨基-苯基）-4-甲基-7,8-亚甲基二氧基-5H -2,3-苯二氮卓（GYKI 52466）完全阻断了环噻嗪增强的海藻酸盐毒性，而环噻嗪增加了NBQX和GYKI 52466对抗海藻酸盐毒性的IC50S。 N-甲基-D-天冬氨酸（NMDA）拮抗剂（+）-5-甲基-10,11-二氢-5H-二苯并[a，d]环庚-5,10-亚胺（MK801）也可以阻断增强环噻嗪的作用海藻酸盐毒性，但仅部分。环乙肼还增加了MK801抗海藻酸盐毒性的IC50。这些数据表明环噻嗪在海藻酸盐诱导的胚胎大鼠海马培养物中的毒性中增强了AMPA优先受体和NMDA受体介导的毒性。

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