Abstract

OBJECTIVE: This experimental study evaluated the pathophysiological association of long-term potentiation (LTP)-mediated synaptic plasticity in tinnitus in 30 BALB/c mice.

MATERIALS and METHODS: Baseline hearing levels and tinnitus perception were examined with startle reflex time and gap detection time measurements using an acoustic stimulus of a 6-kHz pure tone at 90 dB sound pressure level (SPL) on post-natal day 16. The acoustic trauma group was exposed to 6-kHz pure tone at 120 dB SPL on post-natal day 16. On post-natal day 17, the acoustic trauma group underwent re-measurements of hearing levels and tinnitus perception using an acoustic stimulus of 6-kHz pure tone at 100 dB SPL. Fifteen tinnitus-induced and fifteen control subjects were sacrificed on post-natal day 17, and LTP in the dorsal cochlear nuclei of each animal was examined. 

RESULTS: With respect to gap detection time, there were no statistically significant between-group differences; however, there was a statistically significant difference between the pre- and post-trauma period in the acoustic trauma group. Moreover, LTP was significantly higher in the acoustic trauma group than in the control group.

CONCLUSION: The results suggest that LTP underlies tinnitus pathogenesis.