Resting-state Functional MRI Study of Mice with Tinnitus Induced by Traumatic Noise Exposure and Sodium Salicylate Overdose

Tinnitus, a phantom auditory sensation, significantly impacts quality of life and social interactions. While central gain changes, including hyperactivity and increased neural synchrony, have been implicated in tinnitus, the underlying neural mechanisms remain unclear. This study utilized resting-state functional magnetic resonance imaging (rs-fMRI) to investigate the neural basis of tinnitus induced in mice by two distinct methods, traumatic noise exposure and sodium salicylate overdose. Behavioral tests confirmed the successful induction of tinnitus in both groups. rs-fMRI analysis revealed distinct patterns of neural activity in mice with tinnitus compared with control mice. Traumatic noise exposure induced an increase in amplitude of low-frequency fluctuations (ALFF) in the paraflocculus and auditory cortex, as well as a decrease in regional homogeneity (ReHo) in limbic system regions. On the other hand, sodium salicylate overdose led to decreased ALFF and ReHo in the auditory cortex, somatosensory system and limbic system regions. Functional connectivity analysis further highlighted differences between the two models, with traumatic noise exposure affecting connectivity with the inferior colliculus and sodium salicylate overdose affecting connectivity with the medial geniculate body. These findings suggest that traumatic noise exposure and sodium salicylate overdose induce tinnitus through distinct neural mechanisms, potentially involving different neural circuits and pathways. Further research is needed to explore these mechanisms and develop targeted therapies for tinnitus.