环噻嗪可揭示AMPA诱发的大鼠海马突触体中[3H]-L-谷氨酸释放的刺激作用。
Cyclothiazide unmasks AMPA-evoked stimulation of [3H]-L-glutamate release from rat hippocampal synaptosomes.
作者信息
Barnes J M, Dev K K, Henley J M
机构信息
Department of Pharmacology, Medical School, University of Birmingham, Edgbaston.
出版信息
Br J Pharmacol. 1994 Oct;113(2):339-41. doi: 10.1111/j.1476-5381.1994.tb16902.x.
Abstract
The effect of alpha-amino-3-hydroxy-5-methylisoxazolepropionate (AMPA) on Ca(2+)-sensitive, tetrodotoxin (TTX)-insensitive K(+)-stimulated [3H]-L-glutamate release from rat hippocampal synaptosomes was determined. AMPA in the presence, but not in the absence of cyclothiazide, a drug which blocks AMPA receptor desensitization, elicited a dose-dependent increase in K(+)-stimulated [3H]-L-glutamate release but had no effect on basal release. The AMPA/cyclothiazide stimulation was blocked by CNQX and by GYKI 52466, an antagonist at the cyclothiazide site. These results indicate that AMPA receptors are present on presynaptic terminals and suggest that they may play a role in the regulation of neurotransmitter release.
摘要
测定了α-氨基-3-羟基-5-甲基异恶唑丙酸（AMPA）对大鼠海马突触体中钙敏感、河豚毒素（TTX）不敏感的钾离子刺激的[3H]-L-谷氨酸释放的影响。在存在可阻断AMPA受体脱敏的药物环噻嗪的情况下，AMPA可引起钾离子刺激的[3H]-L-谷氨酸释放呈剂量依赖性增加，但对基础释放无影响。AMPA/环噻嗪刺激被CNQX和环噻嗪位点拮抗剂GYKI 52466阻断。这些结果表明AMPA受体存在于突触前终末，并提示它们可能在神经递质释放的调节中发挥作用。
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