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Postnatal Ethanol Exposure Activates HDAC-Mediated Histone Deacetylation, Impairs Synaptic Plasticity Gene Expression and Behavior in Mice.
International Journal of Neuropsychopharmacology ( IF 4.5 ) Pub Date : 2020-03-14 , DOI: 10.1093/ijnp/pyaa017
Madhu Shivakumar 1 , Shivakumar Subbanna 1 , Vikram Joshi 1 , Balapal S Basavarajappa 1, 2, 3, 4
Affiliation  

Alcohol consumption during pregnancy is widespread and contributes to pediatric neurological defects, including hippocampal and neocortex dysfunction, causing cognitive deficits termed fetal alcohol spectrum disorders. However, the critical mechanisms underlying these brain abnormalities remain poorly described.

中文翻译:

出生后乙醇暴露激活 HDAC 介导的组蛋白去乙酰化,损害小鼠的突触可塑性基因表达和行为。

怀孕期间饮酒很普遍,会导致小儿神经系统缺陷,包括海马和新皮质功能障碍,导致认知缺陷,称为胎儿酒精谱系障碍。然而,这些大脑异常背后的关键机制仍然鲜为人知。
更新日期:2020-03-14
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