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[目的]观察注射给予孕期持续摄取酒精母鼠外源性甲状腺素对新生子鼠大脑发育的影响.[方法]选择体质量及一般情况相似的SD孕鼠,用随机数字表法分为正常组、酒精组、酒精+T4组和代理母组.分娩6h后将酒精+T4组母鼠与子鼠分开,每天给予22%(体积分数)酒精,并颈后皮下注射给予5μg/kg甲状腺素.行麻醉后采集心脏血,测定血液中酒精及甲状腺素含量.新生子鼠由代理母组的母鼠养育,分别于出生后0,7,14,21,28 d(P0,P7,P14,P21,P28)采用免疫组织化学染色法观察子鼠大脑中BDNF和TrkB阳性神经细胞的形态及分布.[结果]酒精+T4组血液中酒精含量明显高于正常组(P<0.05),甲状腺素含量明显高于酒精组(P<0.05);P7时酒精+T4组大脑皮质中BDNF和TrkB阳性神经细胞形态及分布与正常组相似,可观察到长而明显突起的成熟的BDNF和TrkB阳性神经细胞,而酒精组始终未出现具有明显突起的成熟的BDNF和TrkB阳性神经细胞.[结论]注射给予孕期持续摄取酒精母鼠外源性甲状腺素可促进后代出生后早期大脑皮质中BDNF及其功能性受体TrkB的合成,促进BDNF和TrkB阳性神经细胞的发育,改善胎儿酒精效果所致低甲状腺素所引起的大脑发育障碍.
[Objective] To observe the effects of administration of exogenous thyroid hormone on the brain development of neonatal rats during pregnancy by alcohol ingestion. [Methods] SD pregnant rats with similar body weight and general conditions were randomly divided into normal group , Alcohol group, alcohol group + T4 group and representative mother group.After 6 hours of labor, the alcohol + T4 group were separated from the rats, and the rats were given 22% (volume fraction) alcohol daily and subcutaneously injected with 5μg / kg thyroxine. Cardiac blood was collected after anesthesia and the content of alcohol and thyroxine in the blood was measured.The neonatal rats were nourished by female rats of the proxy mother group and were respectively fed on 0, 7, 14, 21, 28 d after birth (P0, P7, P14, P21 , P28). Immunohistochemical staining was used to observe the morphous and distribution of BDNF and TrkB positive neurons in the brain of offspring. [Result] The alcohol content in alcohol + T4 group was significantly higher than that in normal group (P <0.05) (P <0.05). The morphology and distribution of BDNF and TrkB positive neurons in the cerebral cortex of alcohol + T4 group at P7 were similar to that of the normal group, and mature BDNF and TrkB positive neurons , Whereas the mature BDNF and Trk with obvious prominence did not appear in alcohol group B positive neurons.Conclusion: Administration of exogenous thyroxine to alcohol maternal rats during pregnancy can promote the synthesis of BDNF and its functional receptor TrkB in early cerebral cortex and promote the development of BDNF and TrkB positive neurons , To improve fetal alcohol-induced hypothyroid hormone-induced brain development disorders.