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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 >The non-competitive AMPA receptor antagonist (GYKI 52466) blocks quisqualate-induced acetylcholine release from the rat hippocampus and striatum: an in vivo microdialysis study.
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The non-competitive AMPA receptor antagonist (GYKI 52466) blocks quisqualate-induced acetylcholine release from the rat hippocampus and striatum: an in vivo microdialysis study.

机译：非竞争性AMPA受体拮抗剂（GYKI 52466）阻止喹喹啉诱导的乙酰胆碱从大鼠海马和纹状体释放：一项体内微透析研究。

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摘要

The effects of the non-N-methyl-D-aspartate (NMDA) agonist quisqualate (QUIS) and selective AMPA/kainate receptor antagonist 1-(aminophenyl)-methyl-7, 8-methyilendioxy-5H-2,3-benzodiazepine (GYKI 52466) on the release of acetylcholine (ACh) from the hippocampus and striatum of freely moving rats were studied by transversal microdialysis. Acetylcholine level in the dialisate was measured by the high performance liquid chromatography (HPLC) method with an electrochemical detector. The QUIS (100 microM) perfused through the striatum induced an increase of extracellular ACh level (250%) which lasted for over 1h and gradually returned to basal values. Local perfusion of GYKI 52466 (10-100 microM) to the striatum did not change the basal release of ACh. GYKI 52466 (10 microM) administered together with QUIS (100 microM) in he striatum antagonized the stimulant effect of QUIS on the ACh release.Local administration of the QUIS (100 microM) through the microdialysis fiber implanted in the hippocampus, caused a long lasting increase of extracellular hippocampal ACh level (360%) which was reversed when the drug was withdrawn from the perfusion solution. The stimulant effect of QUIS was antagonized by concomitant perfusion of GYKI (10 microM). No effect was seen on the basal ACh release when GYKI (10-100 microM) was perfused through the hippocampus.Local perfusion with tetrodotoxin (1 microM) decrease the basal release of ACh and prevented the QUIS-induced increase of ACh both in the hippocampus and striatum.Our in vivo neurochemical results indicate that hippocampal and striatal cholinergic systems are regulated by non-NMDA (probably AMPA) glutamatergic receptors located in the hippocampus and striatum.
机译：非N-甲基-D-天门冬氨酸（NMDA）激动剂喹喹酸酯（QUIS）和选择性AMPA /海藻酸酯受体拮抗剂1-（氨基苯基）-甲基-7，8-甲基亚甲二氧基-5H-2,3-苯并二氮杂（ GYKI 52466）通过横向微透析研究了自由运动大鼠海马和纹状体中乙酰胆碱（ACh）的释放。通过具有电化学检测器的高效液相色谱（HPLC）方法测量透析液中的乙酰胆碱水平。通过纹状体灌注的QUIS（100 microM）导致细胞外ACh水平升高（250％），持续超过1h并逐渐恢复到基础值。 GYKI 52466（10-100 microM）对纹状体的局部灌注不会改变ACh的基础释放。 GYKI 52466（10 microM）与QUIS（100 microM）一起在纹状体中拮抗QUIS对ACh释放的刺激作用.QUIS（100 microM）通过植入海马体的微透析纤维局部给药，导致长期持续从灌注溶液中撤出药物后，细胞外海马ACh水平升高（360％）。伴随灌注GYKI（10 microM）对抗QUIS的刺激作用。当通过海马灌注GYKI（10-100 microM）时，对基础ACh的释放没有影响。河豚毒素（1 microM）的局部灌注降低了ACh的基础释放并阻止了QUIS诱导的海马中ACh的增加。我们体内的神经化学结果表明，海马和纹状体胆碱能系统受到位于海马和纹状体中的非NMDA（可能是AMPA）谷氨酸能受体的调节。

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