We have previously communicated that multisession epidural direct current anodic stimulation (ES) of the auditory cortex (AC) preserves hearing thresholds (Fernández del Campo, 2024) and the loss of neurons in the olivary brainstem efferent system (Alvarado, 2024) after aging. Although it is known that the descending pathway is the main effector for hearing preservation in our age-related hearing loss (ARHL) model, intrinsic mechanisms through which ES preserves cortical regulation must be analyzed. Our hypothesis is that our ES protocol regulates AC activity and prevents alterations in inhibitory circuitry, thereby stabilizing hearing thresholds during aging.To test this hypothesis, after applying our previously tested multisession anodal epidural direct current stimulation protocol in a Wistar rat model, we analyzed auditory cortical evoked potentials and c-fos quantitative immunocytochemistry. Also, effects on the loss of inhibitory interneurons were explored through GAD-67 and Parvalbumin quantitative immunocytochemistry.Compared to young rats, animals with ARHL, exhibit changes in wave amplitude, latency, and morphology of auditory evoked potentials, along with a significant decrease in c-fos, GAD-67, and Parvalbumin immunoreactive neurons in the AC. However, after ES we observed better preserved cortical evoked responses and no substantial changes in c-Fos and inhibitory immunocytochemical markers.These findings suggest that multisession ES induces the stabilization of cochlear responses by preserving AC function and the survival of inhibitory micro-circuitry. Present results can help to design future potential therapeutic strategies for brain ES that may benefit the prevention of presbycusis, one of the most prevalent age-related pathologies.