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Yang G, Lobarinas E, Zhang L, Turner J, Stolzberg D, Salvi R, Sun W
Salicylate induced tinnitus: Behavioral measures and neural activity in auditory cortex of awake rats.
Hear Res. 2007 Apr;226(1-2):244-53. Epub 2006 Aug 14.
Center for Hearing and Deafness, Department of Communicative Disorders and Sciences, University at Buffalo, Buffalo,
NY 14214, United States; Department of Otolaryngology, YueYang Hospital, Shanghai, China.
Neurophysiological studies of salicylate-induced tinnitus have generally been carried out under anesthesia, a condition that abolishes
the perception of tinnitus and depresses neural activity. To overcome these limitations, measurement of salicylate induced tinnitus
were obtained from rats using schedule induced polydipsia avoidance conditioning (SIPAC) and gap pre-pulse inhibition of acoustic
startle (GPIAS). Both behavioral measures indicated that tinnitus was present after treatment with 150 and 250mg/kg of salicylate;
measurements with GPIAS indicated that the pitch of the tinnitus was near 16kHz. Chronically implanted microwire electrode arrays
were used to monitor the local field potentials and spontaneous discharge rate from multiunit clusters in the auditory cortex of awake
rats before and after treatment with 150mg/kg of salicylate. The amplitude of the local field potential elicited with 60dB SPL tone bursts
increased significantly 2h after salicylate treatment particularly at 16-20kHz; frequencies associated with the tinnitus pitch. Field potential
amplitudes had largely recovered 1-2 days post-salicylate when behavioral results showed that tinnitus was absent. The mean spontaneous
spike recorded from the same multiunit cluster pre- and post-salicylate decreased from 22spikes/s before treatment to 14spikes/s 2h
post-salicylate and recovered 1 day post-treatment. These preliminary physiology data suggest that salicylate induced tinnitus is associated
with sound evoked hyperactivity in auditory cortex and spontaneous hypoactivity.