NICOTINE PROTECTS AGAINST MU-OPIOID RECEPTOR ANTAGONISM BY BETA-FUNALTREXAMINE - EVIDENCE FOR NICOTINE-INDUCED RELEASE OF ENDOGENOUS OPIOIDS IN BRAIN
NICOTINE PROTECTS AGAINST MU-OPIOID RECEPTOR ANTAGONISM BY BETA-FUNALTREXAMINE - EVIDENCE FOR NICOTINE-INDUCED RELEASE OF ENDOGENOUS OPIOIDS IN BRAIN
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DOI：
10.1016/0304-3940(90)90491-q
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发表时间：
1990-05-18
影响因子：
2.5
通讯作者：
VANLOON, GR
中科院分区：
文献类型：
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作者：
DAVENPORT, KE;HOUDI, AA;VANLOON, GR
我们假设尼古丁的某些作用是通过内源性阿片类物质介导的。本研究旨在证明尼古丁在大鼠脑中释放内源性阿片类药物。在对照组中，皮下注射吗啡（8 mg/kg）产生镇痛或抗伤害性感受，通过延长甩尾潜伏期来测量。脑室内给药早于24小时β- Funalcipine胺（β- FNA，2.5 μ g），一种使阿片受体不可逆地烷基化的拮抗剂，显著降低（66%）吗啡镇痛作用。在β-羟丙基甲基纤维素之前皮下施用尼古丁（0.1mg/kg）。FNA减弱（31%）了β- FNA用于吗啡镇痛。这些数据支持我们的假设，即由尼古丁释放的内源性阿片样物质与μ-并保护它们免受β-阿片受体的失活。FNA。
We have hypothesized that some effects of nicotine are mediated through endogenous opioids. This study was designed to demonstrate in rats that nicotine releases endogenous opioids in brain. In the control group, subcutaneous morphine (8 mg/kg) produced analgesia or antinociception as measured by prolongation of tail flick latency. Intracerebroventricular administration 24 h earlier of .beta.-funaltrexamine (.beta.-FNA, 2.5 .mu.g), an antagonist which irreversibly alkylates opioid receptors markedly reduced (66%) morphine analgesia. Subcutaneous administration of nicotine (0.1 mg/kg) prior to .beta.-FNA attenuated (31%) the inhibitory effect of .beta.-FNA on morphine analgesia. These data support our hypothesis that endogenous opioids released by nicotine bind to .mu.-opioid receptors in brain and protect them against inactivation by .beta.-FNA.