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γ-氨基丁酸诱导的大鼠体温过低:血清素能和胆碱能机制的参与

GABA-induced hypothermia in rats: involvement of serotonergic and cholinergic mechanisms.

作者信息

Serrano J S, Miñano F J, Sancibrián M

出版信息

Gen Pharmacol. 1986;17(3):327-32. doi: 10.1016/0306-3623(86)90048-0.

Abstract

The effects of gamma-aminobutyric acid (GABA) on body temperature of restrained rats has been studied. GABA (250-1000 mg/kg i.p.) caused a dose-dependent fall in BT of restrained rats at an ambient temperature of 18-22 degrees C. The GABA-induced hypothermic response was attenuated by pretreatment with hexamethonium, p-chlorophenylalanine, methysergide, neostigmine and atropine (% MPE values: 27, 35, 51, 64 and 72 respectively). Pretreatment with methysergide and atropine was more potent than hexamethonium and methysergide in inhibiting the GABA-induced hypothermia (% MPE = 68 and 47 respectively). The antagonism by neostigmine of GABA-induced hypothermia was attenuated by pretreatment with hexamethonium (7.5 mg/kg). Yohimbine and chlorimipramine potentiated GABA hypothermia (% MPE = -82 and -8 respectively). The data indicate that GABA-induced hypothermia may be mediated by serotonin and acetylcholine release. Muscarinic receptors may play an important role in the effect of GABA. The results support the hypothesis that the hypothermia induced by GABA is modulated by nicotinic receptors.

摘要

已研究了γ-氨基丁酸(GABA)对束缚大鼠体温的影响。在18 - 22摄氏度的环境温度下,GABA(腹腔注射250 - 1000毫克/千克)可使束缚大鼠的体温呈剂量依赖性下降。六甲铵、对氯苯丙氨酸、麦角新碱、新斯的明和阿托品预处理可减弱GABA诱导的体温过低反应(最大效应百分比值分别为:27、35、51、64和72)。麦角新碱和阿托品预处理在抑制GABA诱导的体温过低方面比六甲铵和麦角新碱更有效(最大效应百分比分别为68和47)。六甲铵(7.5毫克/千克)预处理可减弱新斯的明对GABA诱导的体温过低的拮抗作用。育亨宾和氯米帕明增强了GABA诱导的体温过低(最大效应百分比分别为 - 82和 - 8)。数据表明,GABA诱导的体温过低可能由5-羟色胺和乙酰胆碱释放介导。毒蕈碱受体可能在GABA的作用中起重要作用。结果支持以下假设:GABA诱导的体温过低受烟碱受体调节。

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