• Mariele Stenzel, Mesbah Alam, Marla Witte, Jonas Jelinek, Nina Armbrecht, Adrian Armstrong, Andrej Kral, Joachim K Krauss, Rüdiger Land, Kerstin Schwabe, and Marie Johne.
• Department of Neurosurgery, Hannover Medical School, Carl-Neuberg-Str. 1, 30625 Hanover, Germany.
• Neuroscience. 2024 Nov 8.

AbstractAge-related hearing loss in humans has been associated with cognitive decline, though the underlying mechanisms remain unknown. We investigated the long-term effects of hearing loss on attention, impulse control, social interaction, and neural activity within medial prefrontal cortex (mPFC) subregions. Hearing loss was induced in adult rats via intracochlear neomycin injection (n = 13), with non-operated rats as controls (n = 10). Rats were tested for motor activity (open field), coordination (Rotarod), and social interaction (including ultrasonic vocalization, USV) before surgery and at weeks 1, 2, 4, 8, 16, and 24 post-surgery. From week 8 on, rats were trained in the five-choice serial reaction time task (5-CSRTT) to assess visuospatial attention and impulse control. Finally, oscillatory neuronal activity in mPFC subregions was recorded with multielectrode arrays during anesthesia, followed by immunohistological staining for NeuN+ and Parvalbumin+ cells. Deafened rats were more active than controls, whereas social interaction and USV were temporarily reduced. They also had difficulties to learn the concept of the 5-CSRTT paradigm and made more incorrect responses. Electrophysiology showed decreased power in theta, alpha, and beta frequency, and enhanced high gamma band in the mPFC in deafened rats, which was most pronounced in the cingulate subregion (Cg1). The number of NeuN+ and Parvalbumin+ cells, however, did not differ between groups. The behavioral deficits together with the altered neuronal activity found in the Cg1 subregion of the mPFC in adult deafened rats may be used as an endophenotype to elucidate the mechanisms behind the cognitive decline seen in older patients with hearing loss.Copyright © 2024. Published by Elsevier Inc.

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