An Overview of the Mechanisms of Abnormal GABAergic Interneuronal Cortical Migration Associated with Prenatal Ethanol Exposure

被引：11

作者：

Shenoda, Botros B. ^{[1
,2
]}

机构：

[1] Drexel Univ, Coll Med, Pharmacol & Physiol, 245 North 15th St,Mail Stop 488, Philadelphia, PA 19102 USA

[2] Assiut Univ, Dept Pharmacol, Coll Med, Assiut, Egypt

来源：

NEUROCHEMICAL RESEARCH | 2017年 / 42卷 / 05期

关键词：

GABAergic Interneurons; GABA; Prenatal Ethanol Exposure; Fetal Alcohol Spectrum Disorders; ATTENTION-DEFICIT HYPERACTIVITY; MEDIAL GANGLIONIC EMINENCE; ALCOHOL SPECTRUM DISORDERS; GABA NEURON MIGRATION; CEREBRAL-CORTEX; CELL-MIGRATION; IN-UTERO; PARVALBUMIN INTERNEURONS; NEOCORTICAL INTERNEURONS; TANGENTIAL MIGRATION;

D O I：

10.1007/s11064-016-2169-5

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

GABAergic Interneuronal migration constitutes an essential process during corticogenesis. Derived from progenitor cells located in the proliferative zones of the ventral telencephalon, newly generated GABAergic Interneuron migrate to their cortical destinations. Cortical dysfunction associated with defects in neuronal migration results in severe developmental consequences. There is growing evidence linking prenatal ethanol exposure to abnormal GABAergic interneuronal migration and subsequent cortical dysfunction. Investigating the pathophysiological mechanisms behind disrupted GABAergic interneuronal migration encountered with prenatal alcohol exposure is crucial for understanding and managing fetal alcohol spectrum disorders. This review explores the molecular pathways regulating GABAergic interneuronal cortical migration that might be altered by prenatal ethanol exposure thus opening new avenues for further research in this topic.

引用

页码：1279 / 1287

页数：9

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