Lugo Joaquin N, Wilson Marlene A, Kelly Sandra J
Department of Psychology, University of South Carolina, Columbia, SC 29208, USA.
Neurotoxicol Teratol. 2006 Mar-Apr;28(2):238-44. doi: 10.1016/j.ntt.2005.12.004. Epub 2006 Feb 2.
This study used a rat model of Fetal Alcohol Syndrome to investigate whether combined prenatal and postnatal ethanol exposure affects met-enkephalin levels in the brains of male and female Long-Evans adult rats. Intragastric ethanol was administered to a group of rats (ET) from gestational day (GD) 1 through 22 and from postnatal day (PD) 2 through 10. The control groups consisted of a nontreated control group (NTC) and an intubated control group (IC) that received the intragastric intubation procedure but no exposure to ethanol. We measured met-enkephalin levels in the prefrontal cortex, nucleus accumbens, hypothalamus, central and basolateral nucleus of amygdala and ventral tegmental area. Met-enkephalin levels in the hypothalamus of male and female ET animals were significantly higher than those in either the NTC or IC animals. Met-enkephalin levels in the central nucleus of the amygdala of male and female ET animals were significantly lower than the levels in the NTC animals. Met-enkephalin levels in the nucleus accumbens of ET females were significantly greater than those in the IC females. These results demonstrate that the combination of prenatal and postnatal ethanol exposure affects basal met-enkephalin levels in specific regions in a sex-specific manner. These changes in met-enkephalin levels may explain how early ethanol exposure affects opioid-regulated behaviors such as social play, sexual behavior, and other social behaviors.
本研究使用胎儿酒精综合征大鼠模型，以探究产前和产后乙醇联合暴露是否会影响成年雄性和雌性Long-Evans大鼠大脑中甲硫氨酸脑啡肽水平。从妊娠第1天（GD1）至22天以及从出生后第2天（PD2）至10天，对一组大鼠（ET组）进行胃内乙醇给药。对照组包括未处理的对照组（NTC组）和接受胃内插管操作但未暴露于乙醇的插管对照组（IC组）。我们测量了前额叶皮质、伏隔核、下丘脑、杏仁核中央核和基底外侧核以及腹侧被盖区中甲硫氨酸脑啡肽的水平。雄性和雌性ET组动物下丘脑中甲硫氨酸脑啡肽水平显著高于NTC组或IC组动物。雄性和雌性ET组动物杏仁核中央核中甲硫氨酸脑啡肽水平显著低于NTC组动物。ET组雌性大鼠伏隔核中甲硫氨酸脑啡肽水平显著高于IC组雌性大鼠。这些结果表明，产前和产后乙醇联合暴露以性别特异性方式影响特定区域的基础甲硫氨酸脑啡肽水平。甲硫氨酸脑啡肽水平的这些变化可能解释了早期乙醇暴露如何影响阿片类物质调节的行为，如社交游戏、性行为和其他社会行为。
