Dose-dependent metabolite changes after ethanol intoxication in rat prefrontal cortex using in vivo magnetic resonance spectroscopy

Louise Carton,Florent Auger,Benjamin Rolland,Olivier Cottencin,Maud Pétrault,Delphine Allorge,Nicolas Durieux,Maeva Kyheng,Renaud Jardri,Régis Bordet

doi:10.1038/s41598-019-47187-4

Abstract

Ethanol disrupts the balance between the excitatory (glutamatergic) and inhibitory (GABAergic) neurotransmission systems. We aimed to assess how acute ethanol intoxication in rats affects the levels of GABA, glutamate and other cerebral metabolites after injection of two different doses of ethanol. One in vivo magnetic resonance spectrum of the prefrontal cortex region was acquired before and six spectra were acquired after intraperitoneal injections of saline or ethanol (1 g/kg or 2 g/kg). Brain kinetics after exposure to ethanol were compared to blood ethanol kinetics. GABA levels significantly decreased after injection of 1 g/kg but not 2 g/kg doses of ethanol. Choline levels, which serve as a marker of alterations in membrane composition, significantly decreased after injection of 2 g/kg but not 1 g/kg doses of ethanol. Acute ethanol intoxication appears to result in specific dose-dependent changes in the GABA level and choline level.

Highlights

Dose-dependent metabolite changes after ethanol intoxication in rat prefrontal cortex using in vivo magnetic resonance spectroscopy
Ethanol has been detected on MR spectra in both humans and animals[5,6,7,8,9,10,11], while recent technical developments allow the identification of GABA
The peaks of ethanol in the blood and within the prefrontal cortex occurred within the first minutes after intraperitoneal ethanol administration (Fig. 1)

Summary

Introduction

Dose-dependent metabolite changes after ethanol intoxication in rat prefrontal cortex using in vivo magnetic resonance spectroscopy. We aimed to assess how acute ethanol intoxication in rats affects the levels of GABA, glutamate and other cerebral metabolites after injection of two different doses of ethanol. It regulates the inhibition/excitation balance that causes long-term depression and long-term potentiation modulations, which modify synaptic transmissions This balance has an important role in the brain plasticity necessary for regulation of behavioral, cognitive, memory and learning functions[1]. A better understanding of the relationship between ethanol concentration and its effects on the GABAergic and glutamatergic systems in the prefrontal cortex appears to be crucial to account for and manage the complex effects of acute ethanol intoxication. Ethanol has been detected on MR spectra in both humans and animals[5,6,7,8,9,10,11], while recent technical developments allow the identification of GABA

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