Changes in GABA and glutamate receptors on auditory cortical excitatory neurons in a rat model of salicylate-induced tinnitus.

Tinnitus is associated with neural hyperactivity, which is regulated by neuronal plasticity in the auditory central system, especially the auditory cortex (AC). Excitatory neurons constitute approximately 70-85% of the total populations of neuronal cells. However, few reports have focused on the AMPA receptor (AMPAR) and the GABA(A) receptor (GABA(A)R) on the excitatory neuron in animal model of tinnitus. In this study, we gave rats a single or long-term of salicylate administrations. The tinnitus-like behavior was assessed by combination of the gap prepulse inhibition of acoustic startle (GPIAS) and the pre-pulse inhibition (PPI) tests. Using immunofluorescent staining, we examined whether the AMPAR and the GABA(A)R on the calcium/calmodulin-dependent protein kinase Il alpha (CaMKII alpha)-labeled excitatory neurons in the auditory cortex underwent changes following salicylate treatment. The rats with 14 days of salicylate administration showed evidence of experiencing tinnitus, while the rats receiving a single dose of salicylate manifested no tinnitus-like behavior. Furthermore, the AMP(A)R and GABA A R responded in a homeostatic manner after a single dose of salicylate while those showing in a Hebbian way after long-term salicylate administration. Thus, the different patterns of plasticity change in cortical excitatory neurons might affect the generating of salicylate-induced tinnitus.