Current therapies for Alcohol Use Disorder (AUD) exhibit significant variability in effectiveness, resulting in high relapse rates. Addressing this challenge requires a precision medicine approach incorporating biomarkers responsive to novel treatments. A promising approach involves bioelectronic devices utilising neuroelectric signatures of impaired prefrontal function, a key feature in AUD resulting in diminished inhibitory control over compulsive behaviour and increased vulnerability to relapse. Thus, we reason that event-related potentials and neural oscillations are valuable biomarkers for pharmacological interventions tailored to rectify AUD-related prefrontal impairments. We examined this hypothesis in an established rat model of alcohol dependence using an epidural neuroprosthetic interface to capture prefrontal resting-state and auditory event-related neural activity during withdrawal and after administering psilocybin, a hallucinogen targeting the serotonin 2A receptor (5-HT2AR), and LY379268, an agonist of the metabotropic glutamate receptor 2 (mGluR2), both recognised to alleviate prefrontal dysfunction and relapse. Electrophysiological impairments resulting from chronic alcohol intake were characterised by reduced P1N1 and N1P2 amplitudes and corresponding oscillatory activity, indicating deficiencies in sensory gating and early attentive filtering. Psilocybin and LY379268 successfully restored these impairments. Moreover, alcohol-dependent animals exhibited a dominance in higher-beta frequencies, indicative of an overaroused state prone to relapse, which particularly psilocybin was able to counteract. In addition, administration of either drug decreased resting-state oscillatory activity, suggesting a soothing effect counteracting neural hyperarousal during withdrawal. These findings provide further support for neuroprosthetic devices based on electrophysiological markers indicative of treatment response, particularly highlighting the efficacy of psychedelic-assisted therapy, and endorse 5-HT2AR-mGluR2-based interventions in AUD.