Premium
Effect of Acute Ethanol Administration on the Hippocampal Region Neural Activity Using a Microelectrode Array
Author(s) -
Zhang Yameng,
Yu Hejuan,
Li Weitao,
Yang Yamin,
Wang Xiao,
Qian Zhiyu
Publication year - 2016
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.13144
Subject(s) - hippocampal formation , local field potential , hippocampus , excitatory postsynaptic potential , electrophysiology , population spike , anesthesia , in vivo , saline , chemistry , medicine , population , neuroscience , pharmacology , biology , inhibitory postsynaptic potential , dentate gyrus , microbiology and biotechnology , environmental health
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 CA 1 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 ( LFP s) 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 LFP s during the entire time course of acute EtOH administration. The correlation between spikes and LFP s suggests that they jointly affect encoding in hippocampus.