放线菌酮可消除百日咳毒素诱导的小脑颗粒神经元谷氨酸释放增加的现象。

Cycloheximide abolishes pertussis toxin-induced increase in glutamate release from cerebellar granule neurones.

作者信息

Cullen G P, Huston E, Dolphin A C

机构信息

Department of Pharmacology, Royal Free Hospital School of Medicine, London, UK.

出版信息

Neurosci Lett. 1994 Jan 17;166(1):17-22. doi: 10.1016/0304-3940(94)90830-3.

DOI:10.1016/0304-3940(94)90830-3

PMID:7910677

Abstract

Release of glutamate from cerebellar granule neurones was stimulated either by adding 50 mM K+ to normal Krebs medium, or by adding 5 mM Ca2+ to neurones continuously depolarised with 50 mM K+ in the absence of Ca2+. Pre-incubation of neurones for 16 h with pertussis toxin (PTX) increased the stimulated glutamate release in both K(+)-stimulated and continuously depolarised neurones. Under both conditions, the PTX-induced increase in release was abolished by cycloheximide. In contrast, in the presence of cycloheximide, PTX still prevented the GABAB agonist (-)-baclofen from inhibiting glutamate release. These results suggest that G-protein ADP-ribosylation by PTX in cerebellar granule neurones may increase synthesis of a protein associated with the L-type calcium channel.

摘要

向正常的 Krebs 培养基中添加 50 mM K⁺，或在无 Ca²⁺的情况下向用 50 mM K⁺持续去极化的神经元中添加 5 mM Ca²⁺，均可刺激小脑颗粒神经元释放谷氨酸。用百日咳毒素（PTX）对神经元进行 16 小时的预孵育，可增加 K⁺刺激的神经元和持续去极化的神经元中受刺激的谷氨酸释放。在这两种条件下，环己酰亚胺均可消除 PTX 诱导的释放增加。相反，在存在环己酰亚胺的情况下，PTX 仍可阻止 GABAB 激动剂（-）-巴氯芬抑制谷氨酸释放。这些结果表明，PTX 在小脑颗粒神经元中对 G 蛋白的 ADP 核糖基化作用可能会增加与 L 型钙通道相关的一种蛋白质的合成。