Abstract

Tinnitus is commonly associated with psychosocial stress. However, it is unclear whether stress alone is sufficient to induce neural alterations resulting in tinnitus. In this study, we investigated the causal role of stress in tinnitus generation by experimentally isolating stress exposure as the sole independent variable in a well-established Mongolian gerbil model. Animals were subjected to repeated, inescapable electric foot shocks over three weeks to create a chronic, repeated stress paradigm. Behavioural, endocrine and histological measures were combined to assess tinnitus perception, stress system activation and cochlear synaptopathy. Repeated stress exposure reliably activated the endocrine stress response, as indicated by transient increases in serum cortisol following specific stress sessions. Basal cortisol levels returned to baseline values after the stress period. Behavioural assessment using gap-prepulse inhibition of the acoustic startle reflex revealed only isolated cases of behavioural signs of tinnitus, which occurred at a frequency consistent with false-positive detection and were evenly distributed between stress-exposed and control animals. Histological analyses revealed that ribbon synapse counts were preserved across the cochlea, with no evidence of stress-induced synaptopathy. No systematic relationships were observed between endocrine activation, behavioural outcomes and the number of inner hair cell ribbon synapses. Taken together, these findings suggest that, in the absence of acoustic trauma, repeated chronic stress is not sufficient to induce tinnitus or inner hair cell synaptopathy. These results argue against a primary causal role of stress alone in tinnitus generation and instead support models in which stress modulates symptom expression or perceptual salience in the context of pre-existing auditory dysfunction.