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

• Published in: Alcoholism, clinical and experimental research clinical and experimental research, 2019-05, Vol.43 (5), p.803-811
• Main Authors: Lagström, Oona, Danielsson, Klara, Söderpalm, Bo, Ericson, Mia, Adermark, Louise
• Format: Article
• Language: English
• Subjects: Addictions; Alcohol; Alcohol use; Alcohols; Animal behavior; Animal cognition; Drinking behavior; Drug addiction; Electrophysiology; Ethanol; Evoked potentials; Excitatory postsynaptic potentials; Mental depression; Neostriatum; Neurobiology; Neuroplasticity; Neurosciences; Neurotransmission; Neurovetenskaper; Nucleus Accumbens; Orbitofrontal Cortex; Prefrontal cortex; Recreational use; Reinforcement; Rodents; Striatum
• ISSN: 0145-6008; 1530-0277
• DOI: 10.1111/acer.14014

Background 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. Methods Male Wistar rats were allowed to voluntarily consume ethanol (EtOH) in an intermittent manner for 2 months, after which ex vivo electrophysiological recordings were performed and data compared with isolated water controls housed in parallel. Results 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 2 days was sufficient to restore neurotransmission in the DLS, while the increase in fEPSP amplitude sustained in the DMS. Conclusions 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. This preclinical study demonstrates how voluntary ethanol consumption produces subregions specific neuroadaptations in cortical and striatal brain regions, which correlates with the amount of ethanol consumed. Interestingly, dorsal striatal subregions appear to be especially vulnerable to ethanol‐induced neuroadaptations and are differentially modulated by ethanol consumption. Considering the role of these brain structures in behavioral actions, ethanolinduced transformations could promote a shift from goal directed towards habitual responding, which may further promote alcohol misuse.