首页 | 本学科首页   官方微博 | 高级检索  
   检索      

中枢阿片神经系统对焦虑情绪的调控作用及其机制探讨
作者姓名:Zhang  HT
作者单位:军事医学科学院毒物药物研究所
摘    要:吗啡依赖大鼠自发戒断后其主动接触时间和突期舔水次数均显著减少,并可被5-HT1A受体激动丁螺环酮和色氨酸羟化酸抑制剂对氯苯丙氨酸所对抗。纳曲酮也可使上述两指标降低,并可被吗啡和PCPA所拮抗、被5-羟色氨酸所增强。

关 键 词:吗啡  纳曲酮  药理学  焦虑  中枢  神经调控

Regulation of the central opioidergic nervous system on the emotional state of anxiety and its possible mechanisms
Zhang HT.Regulation of the central opioidergic nervous system on the emotional state of anxiety and its possible mechanisms[J].Progress in Physiological Sciences,1997,28(1):41-44.
Authors:Zhang H T
Institution:Institute of Pharmacology and Toxicology, Academy of Military Medical Sciences, Beijing.
Abstract:The spontaneous withdrawal from morphine in morphine-dependent rats significantly decreased the duration of active interaction in social interaction test and the number of licks during the shock-punished period in Vogel's conflict procedure, which were attenuated by buspirone, a 5-HT1A agonist, as well as para-chlorophenylalanine (PCPA), an inhibitor of tryptophan hydroxylase. Naltrexone (NTX), a potent opioid receptor antagonist, also dose- and time-dependently reduced both indices mentioned above, which was blocked by morphine or PCPA and was enhanced by 5-hydroxytryptophan, a precursor of 5-HT. In the test of neurotransmitter releases in rat brain slices, both morphine-withdrawal and NTX enhanced high potassium(30mM)-induced 5-HT release in slices of the area of the raphe nucleus. These results suggested that both morphine-withdrawal and NTX produced anxieties in morphine-dependent and normal rats, respectively, which were mediated by the central 5-HTergic neurotransmission. Central opioidergic neurons inhibited 5-HTergic neurons tonically and presynaptically. Such an effect was reduced or blocked by NTX, or during morphine-withdrawal, and 5-HTergic neurons were disinhibited, leading to a state of anxiety.
Keywords:Anxiety  Animal model  Morphine  Withdrawal symptoms  Naltrexone  
本文献已被 CNKI 维普 PubMed 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号