Long-Lasting Neural Circuit Dysfunction Following Developmental Ethanol Exposure

Brain Sciences

Benjamin Sadrian¹  Donald A. Wilson¹ 

[1]Department of Child and Adolescent Psychiatry, New York University Langone School of Medicine, One Park Avenue, Eighth Floor, New York, NY 10128, USA

[2] E-Mail:

关键词: alcohol;    FASD;    neural circuit;    brain development;    excitation/inhibition balance;    neurodegeneration;   

DOI  :  10.3390/brainsci3020704

来源: mdpi

【 摘 要 】

Fetal Alcohol Spectrum Disorder (FASD) is a general diagnosis for those exhibiting long-lasting neurobehavioral and cognitive deficiencies as a result of fetal alcohol exposure. It is among the most common causes of mental deficits today. Those impacted are left to rely on advances in our understanding of the nature of early alcohol-induced disorders toward human therapies. Research findings over the last decade have developed a model where ethanol-induced neurodegeneration impacts early neural circuit development, thereby perpetuating subsequent integration and plasticity in vulnerable brain regions. Here we review our current knowledge of FASD neuropathology based on discoveries of long-lasting neurophysiological effects of acute developmental ethanol exposure in animal models. We discuss the important balance between synaptic excitation and inhibition in normal neural network function, and relate the significance of that balance to human FASD as well as related disease states. Finally, we postulate that excitation/inhibition imbalance caused by early ethanol-induced neurodegeneration results in perturbed local and regional network signaling and therefore neurobehavioral pathology.

【 授权许可】

CC BY   
© 2013 by the authors; licensee MDPI, Basel, Switzerland.