Voluntary Ethanol Intake Produces Subregion-Specific Neuroadaptations in Striatal and Cortical Areas of Wistar Rats.

Abstract

Addiction has been conceptualized as a shift from controlled recreational use toward compulsive and habitual drug-taking behavior. Although the brain reward system is vital for alcohol reward and reinforcement, other neuronal circuits may be involved in controlling long-term alcohol-seeking and drug-taking behaviors. The aim of this study was to outline alcohol-induced neuroplasticity in defined cortical and striatal subregions, previously implicated in alcohol use disorder. Male Wistar rats were allowed to voluntarily consume ethanol (EtOH) in an intermittent manner for 2months, after which exvivo electrophysiological recordings were performed and data compared with isolated water controls housed in parallel. Field potential recordings revealed an increase in field excitatory postsynaptic potentials (fEPSPs) in the dorsomedial striatum (DMS) of rats consuming EtOH, while a depression of evoked potentials was detected in the dorsolateral striatum (DLS). Mean activity in cortical (medial prefrontal cortex, lateral orbitofrontal cortex [OFC]), and accumbal regions (nucleus accumbens [nAc] core/shell) was not significantly altered as compared to water-drinking controls, but a correlation between the amount of alcohol consumed and evoked potentials could be found in both dorsal striatal subregions, OFC, and nAc core. Removal of EtOH for 1 to 2days was sufficient to restore neurotransmission in the DLS, while the increase in fEPSP amplitude sustained in the DMS. These preclinical findings are in line with clinical observations indicating that alcohol produces neurophysiological transformations in dorsal striatal circuits, which in turn may lead to disruptions in decision-making processes that could further promote alcohol misuse.