Differential neural activity and connectivity patterns in rats with and without noise-induced tinnitus

This study investigates the role of central nervous system networks outside the auditory system in the development of tinnitus.

Twenty Sprague-Dawley rats were exposed to 96 dB SPL narrowband noise (right ear, 1 h); nine unexposed rats served as controls. Tinnitus presence was evaluated through gap prepulse inhibition of acoustic startle (GPIAS-PPI), which divided the exposed rats into tinnitus (ET, n = 8) and non-tinnitus (ENT, n = 12) groups. The auditory brainstem response (ABR) was utilized to evaluate hearing thresholds and wave I parameters. Resting-state fMRI (rs-fMRI) revealed significant increases/decreases in resting-state indices, including the amplitude of low-frequency fluctuations (ALFF), regional homogeneity (ReHo), and functional connectivity.

ABR exhibited no intergroup threshold differences. Post-exposure, ET and ENT groups exhibited a decrease in click-evoked wave I amplitude compared to pre-exposure levels, along with an increase in 8 kHz wave I amplitude compared to controls. Rs-fMRI revealed that the ET group had increased ALFF in the entorhinal cortex, amygdala, hippocampus, and superior colliculus, and decreased ALFF in the cingulate and prelimbic cortices. The ENT group showed increased cerebellar activity and decreased basal forebrain activity. ReHo was elevated in the ET group's entorhinal/amygdala and reduced in the cingulate cortex, whereas the ENT group showed reduced basal forebrain/striatum ReHo. ET weakened amygdala-sensory connections and ENT enhanced basal forebrain-cingulate/sensory connectivity.

Noise-exposed rats with/without tinnitus exhibit distinct neural activity/connectivity patterns, supporting a noise-cancellation gating mechanism. Compensatory prelimbic cortex/striatum connectivity may prevent tinnitus in the ENT group. Further research should target noise elimination pathways and the hippocampal/entorhinal roles in "abnormal auditory memory."