Alcohol use disorder (AUD) is a severe chronic condition characterized by compulsive alcohol use, cravings and high relapse rates even after long periods of abstinence. It is suggested that alterations in neuronal network activity, especially in the reward pathway accompany or even mediate relapse behavior. Here we used a DSM-based rat model to map in a first set of experiments neurochemical alterations in the reward pathway during alcohol relapse. Compared to the abstinence condition, we found specific elevation of dopamine levels in the nucleus accumbens shell and the medial prefrontal cortex. We then conducted local field potential (LFP) recordings in these brain sites and observed decreased low-beta oscillatory activity in the nucleus accumbens shell and increased high beta activity in the medial prefrontal cortex. In conclusion, as in comparison with abstinence from alcohol, alcohol relapse is associated with enhanced dopamine levels in the mesolimbic system and an inverse correlation between β oscillatory activity and dopamine availability in the nucleus accumbens shell. These findings suggest that during a relapse situation reduced synchronous oscillatory activity of the local neural population in the nucleus accumbens shell occurs. This local neural population presumably relates to dopaminoceptive medium spiny neurons that show reduced synchronicity during a relapse situation.
Keywords: Alcohol deprivation effect; Alcohol use disorder; Beta band oscillations; Dopamine; Local field potentials; Medial prefrontal cortex; Nucleus accumbens; Relapse.
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