Medina Alexandre E, Ramoa Ary S
Department of Anatomy and Neurobiology, Virginia Commonwealth University School of Medicine, 1101 E Marshall Street, Sanger Hall Room 12-042, Richmond, VA 23298-0709, USA.
Brain Res Dev Brain Res. 2005 Jun 9;157(1):107-11. doi: 10.1016/j.devbrainres.2005.03.012.
Animal models of fetal alcohol syndrome (FAS) have revealed an impairment of sensory neocortex plasticity. Here, we examine whether early alcohol exposure leads to a permanent impairment of ocular dominance plasticity (OD) or to an alteration in the timing of the critical period. Ferrets were exposed to alcohol during a brief period of development prior to eye opening and effects of monocular deprivation examined during early, mid and late critical period. Single-unit electrophysiology revealed markedly reduced OD plasticity at every age examined. This finding provides evidence that early alcohol exposure does not affect the timing or duration of the critical period of OD plasticity and suggests an enduring impairment of neural plasticity in FAS.
胎儿酒精综合征（FAS）的动物模型已揭示感觉新皮质可塑性受损。在此，我们研究早期酒精暴露是否会导致眼优势可塑性（OD）的永久性损伤或关键期时间的改变。雪貂在睁眼之前的短暂发育期间暴露于酒精，并在关键期的早期、中期和晚期检查单眼剥夺的影响。单单位电生理学显示，在每个检查年龄，OD可塑性均显著降低。这一发现证明早期酒精暴露不会影响OD可塑性关键期的时间或持续时间，并提示FAS中神经可塑性存在持久损伤。
