Hearing loss in the elderly has been associated with cognitive impairments and an increased risk of dementia. Social withdrawal due to difficulties in verbal interaction may play an important role. Previous research on deafened rats, ruling out language as a potential confounding factor, showed only initial and mild cognitive deficits during learning, whereas electrophysiological recordings in the prefrontal cortex revealed compromised neuronal activity to some extent. The present study tested whether hearing loss would lead to altered expression of the GABA and dopamine (DA) systems in key regions of the auditory pathway (inferior colliculus, auditory cortex) and the prefrontal cortex.Hearing loss was induced in adult male Sprague-Dawley rats by intracochlear injection of neomycin. Naive and sham-operated rats served as controls. Six months later, the animals were euthanized and their brains were prepared for immunohistological analysis. Parvalbumin (Parv; expressed in GABAergic neurons), tyrosine-hydroxylase (TH; expressed in DAergic neurons), and neuronal nuclei (NeuN) positive neurons were counted in the inferior colliculus, auditory cortex, and medial prefrontal cortex in 10 naive controls, 7 sham-operated controls, and 11 deafened animals.Statistical analysis of the number of Parv, TH, or NeuN positive neurons with a one-way ANOVA showed no significant differences between the deafened rats and sham-lesioned or naive controls (all p>0.1).With the methods used, deafening in adult rats does not lead to neuroanatomical alterations in the auditory pathway and prefrontal cortex despite mild cognitive deterioration shown during behavioral testing.