ISSN 1308-7649 | E-ISSN 2148-3817
Original Article
Assessment of Synaptic Plasticity via Long-Term Potentiation in Young Mice on the Day after Acoustic Trauma: Implications for Tinnitus
1 Department of Ear Nose and Throat, Dokuz Eylül University School of Medicine, İzmir, Turkey  
2 Department of Physiology, Fırat University School of Medicine, Elazığ, Turkey  
3 Department of Ear Nose and Throat, Section of Hearing, Speech and Balance Disorders, Dokuz Eylül University School of Medicine, İzmir, Turkey  
4 Department of Ear Nose and Throat, Fırat University School of Medicine, Elazığ, Turkey  
J Int Adv Otol 2015; 11: 196-201
DOI: 10.5152/iao.2015.1047
Key Words: Tinnitus, noise induced, neuronal plasticity, long-term potentiation, cochlear nucleus, acoustic trauma
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.

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