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Prenatal ethanol exposure increases ethanol intake and reduces C-fos expression in infralimbic cortex of adolescent rats

机译:产前乙醇暴露会增加乙醇摄入并降低青少年大鼠空皮中的C-FOS表达

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摘要

Prenatal ethanol exposure significantly increases later predisposition for alcohol intake, but the mechanisms associated with this phenomenon remain hypothetical. This study analyzed (Experiment 1) ethanol intake in adolescent inbred WKAH/Hok Wistar rats prenatally exposed to ethanol (2.0 g/kg) or vehicle, on gestational days 17-20. Subsequent Experiments (2, 3 and 4) tested several variables likely to underlie the effect of gestational ethanol on adolescent ethanol preference, including ethanol-induced locomotor activation (LMA), ethanol-induced emission of ultrasonic vocalizations (USVs) after exposure to a rough exteroceptive stimulus, and induction of the immediate early gene C-fos in brain areas associated with processing of reward stimuli and with the retrieval and extinction of associative learning. Prenatal ethanol induced a two-fold increase in ethanol intake. Adolescents exhibited significant ethanol-induced LMA, emitted more aversive than appetitive USVs, and postnatal ethanol administration significantly exacerbated the emission of USVs. These effects, however, were not affected by prenatal ethanol. Adolescents prenatally exposed to ethanol as fetuses exhibited reduced neural activity in infralimbic cortex (but not in prelimbic cortex or nucleus accumbens core or shell), an area that has been implicated in the extinction of drug-mediated associative memories. Ethanol metabolism was not affected by prenatal ethanol. Late gestational exposure to ethanol significantly heightened drinking in the adolescent offspring of an inbred rat strain. Ethanol-induced LMA and USVs were not associated with differential ethanol intake due to prenatal ethanol exposure. Prenatal ethanol, however, altered basal neural activity in the infralimbic prefrontal cortex. Future studies should analyze the functionality of medial prefrontal cortex after prenatal ethanol and its potential association with predisposition for heightened ethanol intake. ? 2012 Elsevier Inc.
机译:产前乙醇暴露显着增加了酒精摄入的易感性,但与这种现象相关的机制仍然假设。本研究分析(实验1)在妊娠期17-20天前暴露于乙醇(2.0g / kg)或载体的青少年近交-HAH / HOK Wistar大鼠的乙醇摄入量。后续实验(2,3和4)测试了几种变量,可能使妊娠乙醇对青少年乙醇偏好的影响,包括乙醇诱导的运动激活(LMA),乙醇诱导在暴露于粗糙后的超声声发作(USV)的发射与奖励刺激加工相关的脑区立即早期基因C-FOS诱导诱导刺激,并与联合学习的检索与灭绝。产前乙醇诱导乙醇摄入量增加。青少年表现出显着的乙醇诱导的LMA,比满足USV更厌恶,产后乙醇给药显着加剧了USV的排放。然而,这些效果不受产前乙醇的影响。作为胎儿作为乙醇的前暴露于乙醇的青少年表现出缺陷的皮层(但不在前列腺皮质或核心核心或壳中),这一区域呈现出涉及药物介导的联想存储器的灭绝。乙醇代谢不受产前乙醇的影响。乙醇的晚期妊娠接触显着提高了近期大鼠菌株的青少年后代饮用。由于产前乙醇暴露,乙醇诱导的LMA和USV与差分乙醇摄入无关。然而,产前乙醇改变了内部内部前额叶皮质中的基底神经活性。未来的研究应分析产前乙醇后内侧前额叶皮质的功能及其与高乙醇摄入量高的易感性的潜在关联。还2012年elsevier公司

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  • 作者单位

    Instituto de Investigación Médica M. y M. Ferreyra INIMEC-CONICET Universidad Nacional de Córdoba;

    Instituto de Investigación Médica M. y M. Ferreyra INIMEC-CONICET Universidad Nacional de Córdoba;

    Instituto de Investigación Médica M. y M. Ferreyra INIMEC-CONICET Universidad Nacional de Córdoba;

    Center for Developmental Psychobiology Binghamton University Binghamton NY 13902-6000 United;

    Center for Developmental Psychobiology Binghamton University Binghamton NY 13902-6000 United;

    Instituto de Investigación Médica M. y M. Ferreyra INIMEC-CONICET Universidad Nacional de Córdoba;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 药理学;
  • 关键词

    Adolescent; C-fos; Ethanol; LMA; Prenatal exposure; Ultrasonic vocalization;

    机译:青少年;C-FOS;乙醇;LMA;产前暴露;超声波声;

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