LONG-TERM DEFICITS IN CEREBELLAR GROWTH AND ROTAROD PERFORMANCE OF RATS FOLLOWING BINGE-LIKE ALCOHOL EXPOSURE DURING THE NEONATAL BRAIN GROWTH SPURT
LONG-TERM DEFICITS IN CEREBELLAR GROWTH AND ROTAROD PERFORMANCE OF RATS FOLLOWING BINGE-LIKE ALCOHOL EXPOSURE DURING THE NEONATAL BRAIN GROWTH SPURT
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DOI：
10.1016/0892-0362(91)90029-v
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发表时间：
1991-01-01
影响因子：
2.9
通讯作者：
WEST, JR
中科院分区：
文献类型：
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作者：
GOODLETT, CR;THOMAS, JD;WEST, JR
在新生大鼠脑生长突增期，酒精暴露导致小脑生长受限和神经元耗竭。 本研究探讨了新生儿酒精暴露是否永久限制大脑生长，并诱导成年人的运动表现缺陷。 两组大鼠给予4.5克/公斤的酒精，每天在出生后的第4天至第9天，使用人工饲养程序。 一组在12次每日喂食中的两次中给予10.2%（v/v）的酒精溶液，产生361 mg/dl的峰值BAC。 第二组在四次喂食中给予5.1%（v/v）的酒精溶液，产生187 mg/dl的峰值BAC。 对照组包括人工饲养组和正常饲养组。 所有大鼠在大约405日龄时在旋转棒上进行测试，然后在1-2周后进行灌注。 与对照组相比，10.2%组在获得任务方面明显受损，全脑和小脑重量显着降低。 5.1%的处理还显著限制了全脑和小脑的生长，该组的旋转棒性能介于对照组和10.2%组之间。 成年后小脑的减少和运动表现的缺陷证明了大脑生长突增期间暴饮暴食式酒精暴露的永久性结构和功能后果。
The cerebellum is vulnerable to growth restriction and neuronal depletion induced by alcohol exposure during the brain growth spurt of neonatal rats. This study examined whether neonatal alcohol exposure permanently restricted brain growth and induced motor performance deficits in adults. Two groups of rats were given 4.5 g/kg of alcohol per day during postnatal days 4 through 9, using artificial-rearing procedures. One group was given the alcohol as a 10.2% (v/v) solution in two of the 12 daily feedings, producing peak BACs of 361 mg/dl. The second group was given the alcohol as a 5.1% (v/v) solution in four of the feedings, producing peak BACs of 187 mg/dl. Controls included an artificially reared group and a normally reared group. All rats were tested on a rotarod at approximately 405 days of age, then perfused 1-2 weeks later. The 10.2% group was significantly impaired in acquiring the task and had significant reductions in whole brain and cerebellar weight, compared to controls. The 5.1% treatment also significantly restricted whole brain and cerebellar growth, and rotarod performance of that group was intermediate between the control groups and the 10.2% group. The cerebellar reductions and deficits in motor performance in adulthood demonstrate permanent structural and functional consequences of binge-like alcohol exposure during the brain growth spurt.