Koda H, Hashimoto T, Kuriyama K
Department of Pharmacology, Kyoto Prefectural University of Medicine, Japan.
Eur J Pharmacol. 1989 Mar 29;162(3):501-8. doi: 10.1016/0014-2999(89)90341-5.
The effect of OM-853, a new vincamine analogue, on cerebral dopaminergic neurons was investigated in male Wistar rats. The administration of OM-853 (200 mg/kg p.o.) induced facilitation of the metabolic turnover of dopamine (DA) in all brain areas except the cerebral cortex. Addition of OM-853 enhanced the release of [3H]DA from striatal slices; this release was antagonized by atropine (10(-7) M). However, pretreatment with scopolamine (0.5 mg/kg s.c.) inhibited the enhancement of striatal DA turnover induced by OM-853 administration. OM-853 (10(-4) M) inhibited [3H]quinuclidinyl benzilate binding to muscarinic cholinergic receptors in a striatal particulate fraction more potently than carbachol (10(-4) M). These results suggest that OM-853 may induce facilitation of striatal DA turnover by enhancing DA release via the stimulation of muscarinic cholinergic receptor.
在雄性Wistar大鼠中研究了一种新型长春胺类似物OM - 853对脑多巴胺能神经元的影响。口服给予OM - 853(200mg/kg)可促进除大脑皮层外所有脑区多巴胺(DA)的代谢转换。添加OM - 853可增强纹状体切片中[3H]DA的释放;这种释放可被阿托品(10^(-7)M)拮抗。然而,用东莨菪碱(0.5mg/kg皮下注射)预处理可抑制OM - 853给药诱导的纹状体DA转换增强。OM - 853(10^(-4)M)比卡巴胆碱(10^(-4)M)更有效地抑制纹状体微粒体部分中[3H]喹核醇基苯甲酸酯与毒蕈碱胆碱能受体的结合。这些结果表明,OM - 853可能通过刺激毒蕈碱胆碱能受体增强DA释放,从而促进纹状体DA转换。