Prenatal alcohol exposure (PAE) leads to profound deficits in spatial memory and synaptic and cellular alterations to the hippocampus that last into adulthood. Neurons in the hippocampus called place cells discharge as an animal enters specific places in an environment, establish distinct ensemble codes for familiar and novel places, and are modulated by local theta rhythms. Spatial memory is thought to critically depend on the integrity of hippocampal place cell firing. Therefore, we tested the hypothesis that hippocampal place cell firing is impaired after PAE by performing in vivo recordings from the hippocampi (CA1 and CA3) of moderate PAE and control adult rats. Our results show that hippocampal CA3 neurons from PAE rats have reduced spatial tuning. Second, CA1 and CA3 neurons from PAE rats are less likely to orthogonalize their firing between directions of travel on a linear track and between changes in contextual stimuli in an open arena compared to control neurons. Lastly, reductions in the number of hippocampal place cells exhibiting significant theta rhythmicity and phase precession were observed, which may suggest changes to hippocampal microcircuit function. Together, the reduced spatial tuning and sensitivity to contextual changes provide a neural systems-level mechanism to explain spatial memory impairment after moderate PAE.

产前酒精暴露 (PAE) 会导致海马体空间记忆和突触和细胞改变的严重缺陷，并持续到成年期。当动物进入环境中的特定位置时，海马体中称为位置细胞的神经元会放电，为熟悉的和新奇的地方建立独特的集合代码，并受局部 theta 节律的调节。空间记忆被认为在很大程度上取决于海马位置细胞放电的完整性。因此，我们通过体内试验检验了 PAE 后海马位置细胞放电受损的假设来自中度 PAE 和对照成年大鼠海马体（CA1 和 CA3）的录音。我们的结果表明来自 PAE 大鼠的海马 CA3 神经元的空间调谐减少。其次，与对照神经元相比，来自 PAE 大鼠的 CA1 和 CA3 神经元不太可能使它们在线性轨道上的行进方向之间以及在开放竞技场中的上下文刺激变化之间正交化。最后，观察到表现出显着θ节律和相位进动的海马位置细胞数量减少，这可能表明海马微电路功能发生了变化。总之，减少的空间调整和对环境变化的敏感性提供了一种神经系统级机制来解释中度 PAE 后的空间记忆障碍。