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产前暴露于乙醇后,阿片类而非非阿片类应激诱导的镇痛作用增强。

Opioid but not nonopioid stress-induced analgesia is enhanced following prenatal exposure to ethanol.

作者信息

Nelson L R, Taylor A N, Lewis J W, Branch B J, Liebeskind J C

出版信息

Psychopharmacology (Berl). 1985;85(1):92-6. doi: 10.1007/BF00427329.

Abstract

Two neurochemically distinct forms of stress-induced analgesia were examined in adult rats following prenatal ethanol exposure. Rats were exposed to ethanol during the last 2 weeks of gestation through a liquid diet presented to the dams. Analgesia testing was conducted when the offspring were 150-210 days of age. Two forms of footshock stress were administered; one that resulted in a naloxone-sensitive (opioid-mediated) analgesia and one that resulted in a naloxone-insensitive (nonopioid) form of analgesia. Rats prenatally exposed to ethanol demonstrated significantly enhanced opioid-mediated analgesia, but unaltered nonopioid analgesia compared to controls. These results confirm previous findings that prenatal exposure to ethanol leads to long-term alterations in responding to some, but not all forms of stress. The possibility that prenatal exposure to ethanol leads to perturbations in the endogenous opioid systems is discussed.

摘要

在成年大鼠中,研究了产前乙醇暴露后两种神经化学性质不同的应激诱导镇痛形式。在妊娠的最后2周,通过给母鼠提供液体饮食,使其暴露于乙醇环境中。当子代150 - 210日龄时进行镇痛测试。施加了两种形式的足部电击应激;一种导致纳洛酮敏感(阿片类介导)的镇痛,另一种导致纳洛酮不敏感(非阿片类)的镇痛形式。与对照组相比,产前暴露于乙醇的大鼠表现出显著增强的阿片类介导的镇痛作用,但非阿片类镇痛作用未改变。这些结果证实了先前的发现,即产前暴露于乙醇会导致对某些但不是所有形式的应激反应的长期改变。讨论了产前暴露于乙醇导致内源性阿片系统紊乱的可能性。

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