Prenatal ethanol exposure during the last third of gestation in rat reduces hippocampal NMDA agonist binding site density in 45-day-old offspring.
Prenatal ethanol exposure during the last third of gestation in rat reduces hippocampal NMDA agonist binding site density in 45-day-old offspring.
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大鼠妊娠最后三分之一期间的产前乙醇暴露会降低 45 日龄后代的海马 NMDA 激动剂结合位点密度。
DOI：
10.1016/0741-8329(92)90007-w
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
West,JR
中科院分区：
文献类型：
--
作者：
Savage,DD;Queen,SA;Sanchez,CF;Paxton,LL;Mahoney,JC;Goodlett,CR;West,JR
本文研究了出生前后不同发育时期乙醇暴露对大鼠海马N-甲基-D-天冬氨酸（NMDA）受体结合的影响。通过母体食用3.35%乙醇液体饲料，使胎鼠幼崽在妊娠期间不同时间段暴露于乙醇。在一项单独的实验中，从出生后第4天（PD）至PD 10天，通过胃内饲管向新生幼仔喂食2.51 g乙醇/kg体重/天。这两种乙醇给药模式产生的母体和幼仔血液乙醇浓度平均峰值分别为39 mg/dl和57 mg/dl。在45日龄时，处死每个处理组的后代，使用体外放射组织化学技术测量海马NMDA敏感性[3 H]-谷氨酸结合位点密度。如前所述，与自由进食或成对进食对照组相比，整个妊娠期产前乙醇暴露导致齿状回、海马CA 1区和背海马结构下托顶端树突区NMDA敏感[3 H]-谷氨酸结合位点减少。仅在妊娠前半期暴露于乙醇的大鼠中，NMDA敏感性[3 H]-谷氨酸结合与对照组无差异。妊娠后半期或妊娠后三分之一期间的产前乙醇暴露导致NMDA敏感性[3 H]-谷氨酸结合位点减少，与整个妊娠期间暴露于乙醇的大鼠中观察到的结合位点减少相当。出生后乙醇暴露大鼠海马NMDA敏感[3 H]-谷氨酸结合位点密度与哺乳或胃造口术对照组无差异。这些结果表明，乙醇诱导的海马NMDA受体结合减少的脆弱性的关键时期发生在大鼠妊娠的最后三分之一，这在人类海马发育方面，是一段时间大致相当于人类妊娠的第五个月和第六个月。
The effect of ethanol exposure during different periods of prenatal or postnatal development on hippocampal N-methyl-D-aspartate (NMDA) receptor binding was studied in rat. Fetal rat pups were exposed to ethanol for different periods of time during gestation via maternal consumption of a 3.35% ethanol liquid diet. In a separate experiment, neonatal pups were fed 2.51 g ethanol/kg body weight/day from Postnatal Day (PD) 4 to PD 10 via intragastric feeding tube. These two ethanol administration paradigms produced average peak maternal and pup blood ethanol concentrations of 39 mg/dl and 57 mg/dl, respectively. At 45 days of age, offspring from each treatment group were sacrificed for measurements of hippocampal NMDA-sensitive [3H]-glutamate binding site density using in vitro radiohistochemical techniques. As observed previously, prenatal ethanol exposure throughout gestation resulted in NMDA-sensitive [3H]-glutamate binding site reductions in the apical dendritic field regions of dentate gyrus, hippocampal CA1and subiculum of dorsal hippocampal formation compared to the ad lib or pair-fed control groups. NMDA-sensitive [3H]-glutamate binding was not different than control in rats exposed to ethanol during the first half of gestation only. Prenatal ethanol exposure during the last half or the last third of gestation resulted in NMDA-sensitive [3H]-glutamate binding site reductions comparable to the binding site reductions observed in rats exposed to ethanol throughout gestation. Hippocampal NMDA-sensitive [3H]-glutamate binding site density in postnatal ethanol-exposed rats was not different than the suckling or gastrostomy control groups. These results suggest that the critical period of vulnerability to ethanol-induced reductions in hippocampal NMDA receptor binding occurs during the last third of gestation in rat, which, in terms of human hippocampal development, is a period of time roughly equivalent to the fifth and six months of human gestation.
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影响因子：
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作者：
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DOI：
10.15288/jsa.1981.42.547
发表时间：
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期刊：
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