Effect of Acute Ethanol Administration on the Hippocampal Region Neural Activity Using a Microelectrode Array.
Effect of Acute Ethanol Administration on the Hippocampal Region Neural Activity Using a Microelectrode Array.
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DOI：
10.1111/acer.13144
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发表时间：
2016-07
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影响因子：
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通讯作者：
Yameng Zhang;Hejuan Yu;Weitao Li;Yamin Yang;Xiao Wang;Z. Qian
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文献类型：
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作者：
Yameng Zhang;Hejuan Yu;Weitao Li;Yamin Yang;Xiao Wang;Z. Qian
由于已知急性乙醇（EtOH）给药通过损害海马功能来影响认知过程，因此需要研究乙醇暴露后海马的电生理反应。为了模拟体内条件，我们动态记录和分析了神经元群体的临界放电特征，特别是在海马区，在急性乙醇给药前后。方法将微电极插入21只癌症研究所小鼠的海马CA 1区。将小鼠分为3组，包括EtOH注射组（1.5g/kg）、盐水注射组（1.5g/kg）和不接受注射的阴性对照组。采用数据采集系统检测急性乙醇给药后的局部场电位（LFPs）和峰电位。在60 min时采集各组动物体内的多通道电生理信号，分析放电率和小波熵（WE）。结果注射后20 min，放电频率开始下降，40 ~ 60 min逐渐恢复。相反，注射后20分钟，WE增加最大，然后从40到60分钟恢复正常（p < 0.05）。在酒精暴露20分钟后也观察到θ和α振荡的相对能量的显著变化，并且在60分钟时恢复（p < 0.05）。结论：乙醇对海马的作用机制主要是通过抑制兴奋性神经元而阻断神经递质。在急性乙醇给药的整个时间过程中，海马棘波的变化与LFPs的变化一致。棘波和LFPs之间的相关性表明它们共同影响海马的编码。
BACKGROUND Because acute ethanol (EtOH) administration is known to influence cognitive processes by impairing hippocampal function, electrophysiological responses of the hippocampus following EtOH exposure warrant investigation. To mimic in vivo conditions, we recorded and analyzed critical firing characteristics of the neuronal population dynamically, particularly in the hippocampal region, before and after acute EtOH administration. METHODS Microelectrodes were inserted in the hippocampus CA1 region of 21 Institute of Cancer Research mice. The mice were divided into 3 groups, including an EtOH injection group (1.5 g/kg), a saline injection group (1.5 g/kg), and a negative control group that received no injection. A data acquisition system was employed to detect the local field potentials (LFPs) and spike potentials following acute EtOH administration. Various multichannel electrophysiological signals were collected in vivo in each group at 60 minutes, from which the firing rate and wavelet entropy (WE) were analyzed further. RESULTS Firing rates began to decline at 20 minutes postinjection and then gradually recovered from 40 to 60 minutes. In contrast, 20 minutes post-injection, WE increased maximally and then returned to normal from 40 to 60 minutes (p < 0.05). Pronounced changes in the relative energy of theta and alpha oscillations were also observed after 20 minutes of alcohol exposure and recovery occurred by 60 minutes (p < 0.05). CONCLUSIONS A major mechanism of EtOH's action on the hippocampus is neurotransmitter blocking in the form of excitatory neuron inhibition in vivo. Changes in hippocampal spikes coincided with changes in LFPs during the entire time course of acute EtOH administration. The correlation between spikes and LFPs suggests that they jointly affect encoding in hippocampus.