Abstract
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 invivo conditions, we recorded and analyzed critical firing characteristics of the neuronal population dynamically, particularly in the hippocampal region, before and after acute EtOH administration. 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 (1.5g/kg), a saline injection group (1.5g/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 invivo in each group at 60minutes, from which the firing rate and wavelet entropy (WE) were analyzed further. Firing rates began to decline at 20 minutes postinjection and then gradually recovered from 40 to 60 minutes. In contrast, 20minutes post-injection, WE increased maximally and then returned to normal from 40 to 60minutes (p<0.05). Pronounced changes in the relative energy of theta and alpha oscillations were also observed after 20minutes of alcohol exposure and recovery occurred by 60minutes (p<0.05). A major mechanism of EtOH's action on the hippocampus is neurotransmitter blocking in the form of excitatory neuron inhibition invivo. 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.
Published Version
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