Shenoda Botros B
Pharmacology and Physiology, Drexel University College of Medicine, 245 North 15th Street, Mail Stop 488, Philadelphia, PA, 19102, USA.
Department of Pharmacology, Assiut University College of Medicine, Assiut, Egypt.
Neurochem Res. 2017 May;42(5):1279-1287. doi: 10.1007/s11064-016-2169-5. Epub 2017 Feb 3.
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.
γ-氨基丁酸能中间神经元迁移是皮质发生过程中的一个重要过程。新生成的γ-氨基丁酸能中间神经元起源于腹侧端脑增殖区的祖细胞，迁移至其在皮质的目的地。与神经元迁移缺陷相关的皮质功能障碍会导致严重的发育后果。越来越多的证据表明，产前乙醇暴露与γ-氨基丁酸能中间神经元迁移异常及随后的皮质功能障碍有关。研究产前酒精暴露导致的γ-氨基丁酸能中间神经元迁移中断背后的病理生理机制，对于理解和管理胎儿酒精谱系障碍至关重要。本综述探讨了可能因产前乙醇暴露而改变的调节γ-氨基丁酸能中间神经元皮质迁移的分子途径，从而为该主题的进一步研究开辟了新途径。
