Department of Neurosciences, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131-0001, USA.
J Neurosci. 2010 May 12;30(19):6776-81. doi: 10.1523/JNEUROSCI.5405-09.2010.
Fetal alcohol spectrum disorder (FASD) is associated with learning and memory alterations that could be, in part, a consequence of hippocampal damage. The CA3 hippocampal subfield is one of the regions affected by ethanol (EtOH), including exposure during the third trimester-equivalent (i.e., neonatal period in rats). However, the mechanism of action of EtOH is poorly understood. In CA3 pyramidal neurons from neonatal rats, dendritic BDNF release causes long-term potentiation of the frequency of GABAA receptor-mediated spontaneous postsynaptic currents (LTP-GABAA) and this mechanism is thought to play a role in GABAergic synapse maturation. Here, we show that short- and long-term exposure of neonatal male rats to low EtOH concentrations abolishes LTP-GABAA by inhibiting L-type voltage-gated Ca2+ channels. These findings support the recommendation that even light drinking should be avoided during pregnancy.
胎儿酒精谱系障碍（FASD）与学习和记忆改变有关，这在一定程度上可能是海马损伤的结果。CA3 海马亚区是受乙醇（EtOH）影响的区域之一，包括在相当于第三个三个月（即大鼠的新生期）期间的暴露。然而，乙醇的作用机制尚不清楚。在新生大鼠的 CA3 锥体神经元中，树突状 BDNF 释放导致 GABAA 受体介导的自发性突触后电流的频率长时程增强（LTP-GABAA），并且认为该机制在 GABA 能突触成熟中起作用。在这里，我们表明，新生雄性大鼠短期和长期暴露于低 EtOH 浓度会通过抑制 L 型电压门控 Ca2+通道来消除 LTP-GABAA。这些发现支持了即使在怀孕期间也应避免轻度饮酒的建议。
