Gestational naltrexone ameliorates fetal ethanol exposures enhancing effect on the postnatal behavioral and neural response to ethanol.
Gestational naltrexone ameliorates fetal ethanol exposures enhancing effect on the postnatal behavioral and neural response to ethanol.
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DOI：
10.1258/ebm.2012.012132
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发表时间：
2012-10
期刊：
影响因子：
--
通讯作者：
Youngentob LM
中科院分区：
文献类型：
--
作者：
Youngentob SL;Kent PF;Youngentob LM
妊娠期暴露于乙醇和青少年乙醇滥用之间的关联是明确的。最近的动物研究支持胎儿乙醇经验诱导的化学感觉可塑性的作用，有助于这一观察。在此之前，我们建立了胎儿乙醇暴露，提供通过一个母亲的饮食在整个妊娠期，调整神经反应的外周嗅觉系统的早期出生后的大鼠乙醇的气味。这与对其他气味的反应性丧失有关。对乙醇气味的本能行为反应也得到了增强。重要的是，在相同的动物中评估时，对乙醇气味的反应改变和乙醇亲和力增加之间存在显着的贡献联系。在这里，我们测试了神经和行为嗅觉可塑性，以及它们与乙醇摄入量增加的关系，是否仅仅是暴露于乙醇的结果，或者是否需要动物将乙醇的增强特性与其气味属性联系起来。在后一方面，阿片系统在乙醇的强化方面的调解（或调节）中是重要的。为了在出生前阻断内源性阿片类药物，妊娠大鼠从妊娠第6 - 21天开始每天腹腔内给予阿片类药物拮抗剂纳洛酮，同时通过饮食给予乙醇。相对于对照后代，我们发现，妊娠期暴露于纳洛酮改善了出生后对乙醇气味和出生后药物亲和力的行为反应。我们的研究结果支持这一命题，即在子宫内乙醇诱导的嗅觉可塑性（及其与出生后摄入量的关系）需要，至少部分地，乙醇的气味质量和其加强方面之间的关联配对。我们还发现了提示性证据，胎儿纳洛酮改善了妊娠期乙醇暴露对非胎儿暴露气味的神经反应的不良影响。因此，妊娠纳洛酮也可能对嗅觉发育具有神经保护和/或神经增殖作用。
The association between gestational exposure to ethanol and adolescent ethanol abuse is well established. Recent animal studies support the role of fetal ethanol experience-induced chemosensory plasticity as contributing to this observation. Previously, we established that fetal ethanol exposure, delivered through a dam’s diet throughout gestation, tuned the neural response of the peripheral olfactory system of early postnatal rats to the odor of ethanol. This occurred in conjunction with a loss of responsiveness to other odorants. The instinctive behavioral response to the odor of ethanol was also enhanced. Importantly, there was a significant contributory link between the altered response to the odor of ethanol and increased ethanol avidity when assessed in the same animals. Here, we tested whether the neural and behavioral olfactory plasticity, and their relationship to enhanced ethanol intake, is a result of the mere exposure to ethanol or whether it requires the animal to associate ethanol’s reinforcing properties with its odor attributes. In this later respect, the opioid system is important in the mediation (or modulation) of the reinforcing aspects of ethanol. To block endogenous opiates during prenatal life, pregnant rats received daily intraperitoneal administration of the opiate antagonist naltrexone from gestational day 6–21 jointly with ethanol delivered via diet. Relative to control progeny, we found that gestational exposure to naltrexone ameliorated the enhanced postnatal behavioral response to the odor of ethanol and postnatal drug avidity. Our findings support the proposition that in utero ethanol-induced olfactory plasticity (and its relationship to postnatal intake) requires, at least in part, the associative pairing between ethanol’s odor quality and its reinforcing aspects. We also found suggestive evidence that fetal naltrexone ameliorated the untoward effects of gestational ethanol exposure on the neural response to non-fetal-exposure odorants. Thus, gestational naltrexone may also have a neuroprotective and/or neuroproliferative impact on olfactory development.
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影响因子：
2.9
作者：
BONTHIUS, DJ;WEST, JR
通讯作者：
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影响因子：
2.3
作者：
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5.1
作者：
Eade, Amber M.;Sheehe, Paul R.;Youngentob, Steven L.
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作者：
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作者：
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