GESTATIONAL COCAINE EXPOSURE INCREASES OPIATE RECEPTOR-BINDING IN WEANLING OFFSPRING

GESTATIONAL COCAINE EXPOSURE INCREASES OPIATE RECEPTOR-BINDING IN WEANLING OFFSPRING
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DOI:
10.1016/0165-3806(91)90098-4
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发表时间:
1991-04-24
期刊:
DEVELOPMENTAL BRAIN RESEARCH
影响因子:
--
通讯作者:
SPEAR, LP
SPEAR, LP
中科院分区:
其他
文献类型:
--
作者:
CLOW, DW;HAMMER, RP;SPEAR, LP

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怀孕期间使用可卡因会对后代产生多种不良影响。众所周知,妊娠期接触可卡因会影响发育中的多巴胺系统,但其他神经化学系统也可能面临风险。在妊娠第 8 天和第 20 天之间暴露于可卡因(0、10、20 或 40 mg/kg/天,皮下注射)的 21 日龄雄性大鼠的大脑中,检查了用[H-3]纳洛酮标记的阿片受体的区域密度。妊娠期可卡因暴露以剂量依赖的方式显着增加了多巴胺能末端(例如伏核、内侧前额叶)的标记。皮质、嗅结节和尾壳核)、边缘区(例如基底外侧杏仁核、外侧缰核、海马、齿状回、内嗅和扣带皮层)和新皮质(例如体感和运动皮质)区域,但对间脑或脑干区域影响不大。结果表明药物诱导的多巴胺系统改变可以调节大脑中阿片类药物系统的功能联系。此外,妊娠期接触可卡因会导致某些大脑区域的阿片受体标记发生长期变化。这些结果的影响尚不确定。然而,这种对内源性阿片类药物系统的影响可能会导致发育迟缓、认知或运动功能障碍。
The use of cocaine during pregnancy produces a variety of adverse effects in offspring. Gestational cocaine exposure is known to affect developing dopamine systems, but other neurochemical systems may also be at risk. Regional density of opiate receptors labeled with [H-3]naloxone was examined in the brains of 21-day-old male rats exposed to cocaine (0, 10, 20, or 40 mg/kg/day s.c.) between gestation days 8 and 20. Gestational cocaine exposure significantly increased labeling in a dose-dependent fashion in dopaminergic terminal (e.g. the nucleus accumbens, medial prefrontal cortex, olfactory tubercle, and caudatoputamen), limbic (e.g. basolateral amygdaloid nucleus, lateral habenula, hippocampus, dentate gyrus, entorhinal and cingulate cortices) and neocortical (e.g. somatosensory and motor cortices) regions, but had little effect in diencephalic or brainstem regions. The results suggest a functional linkage whereby drug-induced alteration of dopamine systems can regulate developing opioid systems in the brain. Moreover, gestational cocaine exposure produced long-lasting changes of opiate receptor labeling in certain brain regions. The implications of these results are uncertain. However, such effects on endogenous opioid systems could contribute to a developmental delay, cognitive or motor dysfunction.