Suppr超能文献

介导可乐定诱导发育中大鼠运动活动减少的中枢α-肾上腺素能受体的药理学特性

Pharmacological characterization of central alpha-adrenoceptors which mediate clonidine-induced locomotor hypoactivity in the developing rat.

作者信息

Nomura Y, Oki K, Segawa T

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1980 Feb;311(1):41-4. doi: 10.1007/BF00500300.

Abstract

The present experiment was designed to pharmacologically characterize receptors which mediate the clonidine-induced locomotor change in the developing rat. A subcutaneous injection of clonidine (0.78 mumol/kg) produced locomotor hyperactivity in 7-day-old rats but hypoactivity in 20-day-old rats. Phenoxybenzamine (1.5 mumol/kg, 5.9 mumol/kg and 15 mumol/kg) decreased spontaneous activity in a dose-dependent manner but did not antagonize clonidine-induced hypoactivity in 20-day-old rats. By contrast, the significant reversal of the clonidine-induced hypoactivity by pretreatment with phentolamine (1.6 mumol/kg and 6.3 mumol/kg), yohimbine (1.3 mumol/kg and 5.1 mumol/kg) and piperoxan (7.4 mumol/kg) was observed at such doses when the blockers did not cause any hypoactivity by themselves. It is suggested that clonidine could induce locomotor hypoactivity by activating presynaptic (alpha 2-type) alpha-adrenoceptors in the CNS of 20-day-old rat.

摘要

本实验旨在从药理学角度对介导可乐定引起发育中大鼠运动变化的受体进行表征。皮下注射可乐定(0.78微摩尔/千克)可使7日龄大鼠出现运动性多动,但使20日龄大鼠出现运动性少动。酚苄明(1.5微摩尔/千克、5.9微摩尔/千克和15微摩尔/千克)以剂量依赖方式降低自发活动,但不拮抗可乐定引起的20日龄大鼠运动性少动。相比之下,当酚妥拉明(1.6微摩尔/千克和6.3微摩尔/千克)、育亨宾(1.3微摩尔/千克和5.1微摩尔/千克)和哌泊昔生(7.4微摩尔/千克)本身不引起任何运动性少动时,在这些剂量下观察到其预处理能显著逆转可乐定引起的运动性少动。提示可乐定可通过激活20日龄大鼠中枢神经系统中的突触前(α2型)α-肾上腺素能受体诱导运动性少动。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验