Low concentrations of alcohol inhibit BDNF-dependent GABAergic plasticity via L-type Ca2+ channel inhibition in developing CA3 hippocampal pyramidal neurons.
Low concentrations of alcohol inhibit BDNF-dependent GABAergic plasticity via L-type Ca2+ channel inhibition in developing CA3 hippocampal pyramidal neurons.
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DOI：
10.1523/jneurosci.5405-09.2010
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发表时间：
2010-05-12
期刊：
影响因子：
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通讯作者：
Valenzuela CF
中科院分区：
文献类型：
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作者：
Zucca S;Valenzuela CF
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，包括在妊娠第三个月（即大鼠的新生儿期）期间的暴露。然而，人们对 EtOH 的作用机制知之甚少。在新生大鼠的 CA3 锥体神经元中，树突状 BDNF 的释放导致 GABAA 受体介导的自发突触后电流 (LTP-GABAA) 频率的长期增强，并且这种机制被认为在 GABA 能突触成熟中发挥作用。在这里，我们发现，新生雄性大鼠短期和长期暴露于低浓度 EtOH 会通过抑制 L 型电压门控 Ca2+ 通道 (VGCC) 来消除 LTP-GABAA。这些发现支持了这样的建议：在怀孕期间即使少量饮酒也应避免。
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 3rd 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 (VGCCs). These findings support the recommendation that even light drinking should be avoided during pregnancy.