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首页> 外文期刊>The European Journal of Neuroscience >Lasting reduction in mesolimbic dopamine neuronal activity after morphine withdrawal.
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Lasting reduction in mesolimbic dopamine neuronal activity after morphine withdrawal.

机译：吗啡戒断后中脑边缘多巴胺神经元活性持续降低。

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The activity of mesolimbic dopaminergic neurons was investigated in rats at various times after a chronic regimen of morphine, which produced, upon suspension, a marked somatic withdrawal syndrome. Single-cell extracellular recording techniques, coupled with antidromic identification from the nucleus accumbens, were used to monitor neuronal activity while behavioural observations allowed quantification of the somatic signs of morphine withdrawal. Temporal correlation of electrophysiological indices, such as firing rate and burst firing, with scores obtained through behavioural assessments proved negative, in that somatic signs were pronounced at 24 h after suspension of treatment and then subsided to control values at 72 h after the last morphine injection. In contrast, the firing rate and burst firing of mesolimbic dopaminergic neurons were found to be reduced at 1, 3 and 7 days after morphine withdrawal. After 14 drug-free days, electrophysiological analysis revealed an apparent normalization of various parameters. However, at this time, intravenous administration of morphine produced an increment of electrical activity which was significantly higher than that obtained in control (saline treated) rats. Further, administration of the opiate antagonist naltrexone, administered without prior morphine, at 3, 7 and 14 days after the last morphine administration, failed to alter dopaminergic neuronal activity. The results indicate: (i) that the activity of mesolimbic dopaminergic neurons remains reduced well after somatic signs of withdrawal have disappeared; (ii) after 14 days of withdrawal, the augmented magnitude of the electrophysiological response to exogenous morphine suggests an increased sensitivity of opiate receptors; and (iii) the lack of relationship between dopaminergic activity and somatic signs of withdrawal corroborates the notion that dopaminergic activity in the mesolimbic system does not participate in the neurobiological mechanisms responsible for somatic withdrawal. The present results may be relevant to the phenomenon of drug addiction in humans and consequent relapse after drug-free periods.
机译：在慢性吗啡治疗后的不同时间，对大鼠中脑边缘多巴胺能神经元的活性进行了研究，吗啡在悬浮后会产生明显的躯体停药综合征。单细胞细胞外记录技术，结合伏伏核的抗体质鉴定，可用于监测神经元活动，而行为观察则可定量吗啡戒断的体征。电生理指标的时间相关性，例如放电速率和爆发放电，与通过行为评估获得的分数呈负相关，因为在停药后24 h体细胞体征明显，然后在最后一次吗啡注射后72 h逐渐降至对照值。相反，发现吗啡戒断后第1、3和7天中脑边缘多巴胺能神经元的放电速率和爆发放电降低。在无药14天后，电生理分析显示各种参数均出现了明显的正常化。然而，此时，吗啡的静脉内给药产生的电活性增加明显高于在对照（盐水处理）大鼠中获得的电活性。此外，在最后一次吗啡给药后第3、7和14天，鸦片拮抗剂纳曲酮的给药在没有先用吗啡的情况下给药，未能改变多巴胺能神经元活性。结果表明：（i）体细胞戒断症状消失后，中脑边缘的多巴胺能神经元的活性仍然降低; （ii）停药14天后，对外源吗啡的电生理反应幅度增加，表明阿片受体的敏感性增加; （iii）多巴胺能活动与躯体退缩体征之间缺乏联系，这证实了中脑边缘系统中的多巴胺能活动不参与引起体细胞退缩的神经生物学机制。目前的结果可能与人类的药物成瘾现象以及无药期后复发有关。

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