Acute Effects of Ethanol on Hippocampal Spatial Representation and Offline Reactivation.

Kosaku Miyake,Yu Shikano,Yuji Ikegaya,Takuya Sasaki,Saichiro Yagi,Yuki Aoki

doi:10.3389/fncel.2020.571175

Abstract

Acute alcohol exposure impairs hippocampus-dependent spatial memory. However, there is little evidence for the effects of ethanol on the spike patterns of hippocampal cell populations. Here, we examined how the spatial firing patterns of place cells, neurons that encode specific locations, were altered in rats that were intraperitoneally injected with 1.5 g/kg ethanol. Ethanol administration partly reduced or abolished place-selective spiking of a subset of place cells during running periods in a spatial task, whereas a subset of place fields newly emerged, suggesting a partial reorganization of hippocampal spatial maps by ethanol. On the other hand, ethanol administration did not significantly alter the frequency of hippocampal sharp-wave ripple (SWRs) and synchronous spike patterns during resting periods, suggesting that offline memory consolidation and retrieval mechanisms underpinned by hippocampal neuronal synchronization are not strongly affected by ethanol. These results indicate that acute ethanol intake mainly affects the encoding of external information but has little impact on internal memory processing.

Highlights

Acute ethanol overconsumption causes marked impairment in a variety of brain functions, including cognition, learning, and memory (Acheson et al, 1998), which have been well replicated in laboratory rodent animals
These behavioral changes are likely explained by several mechanisms outside the hippocampus, including ataxia mediated by the motor system and cerebellum, decreased attention mediated by widespread neocortical and subcortical regions, and altered cerebral blood flow through changes in systemic blood pressure
The hippocampus has been implicated as a brain region involved in these ethanol effects (Ryabinin, 1998; White et al, 2000; Kutlu and Gould, 2016)

Summary

Introduction

Acute ethanol overconsumption causes marked impairment in a variety of brain functions, including cognition, learning, and memory (Acheson et al, 1998), which have been well replicated in laboratory rodent animals. In vivo electrophysiological recordings have revealed that ethanol administration suppresses cellular activity in the medial septum (Givens, 1996), increases the spike rates of dopamine neurons in the ventral tegmental area (VTA; Gessa et al, 1985; Burkhardt and Adermark, 2014), and alters the firing patterns of distinct types of neurons in the central amygdala (Herman and Roberto, 2016) All this evidence indicates that unlike those of compounds that target a single molecule, the mechanisms underlying ethanol-induced changes in hippocampal functions are highly complex, and ethanol-induced hippocampusdependent behavior is associated with a myriad combination of changes in neuronal activity in the intrahippocampal circuit and extrahippocampal regions (Abrahao et al, 2017). To elucidate the precise mechanisms underlying ethanol-related behavior, further studies are required to examine how integrated ethanol-sensitive mechanisms lead to alterations in neuronal spike dynamics in the hippocampus

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