Expression of COX-2 and NMDA receptor genes at the cochlea and midbrain in salicylate-induced tinnitus.

Abstract

The expression of the genes for cyclooxygenase (COX) and NMDA receptor (NR) has seldom been reported in tinnitus. We hypothesized that expression of COX-2 and NR was altered in the cochlea and midbrain in salicylate-induced tinnitus. Experimental study on mice. We evaluated the tinnitus score and mRNA expression levels of COX-2 and NR subtype 2B (NR2B) in the cochlea and midbrain in response to intraperitoneal injections of salicylate for 4 days. At day 4 of tinnitus induction, the mean weights of the whole body and midbrain did not change greatly in both control and salicylate groups. The tinnitus score was not elevated from day 1 to day 4 in the control group, but increased day by day in the salicylate group. The mRNA expression level of COX-2 decreased slightly in the salicylate group in the cochlea (1.1 ± 0.33 vs. 1.3 ± 0.49, P = .0752) and in the midbrain (0.9 ± 0.10 versus 1.0 ± 0.35, P = .0489). Inversely, the expression levels of the NR2B gene increased moderately in the salicylate group in the cochlea (3.7 ± 0.47 versus 2.3 ± 1.13, P < 0.0001) and in the midbrain (1.6 ± 0.64 versus 1.0 ± 0.44, P = .0007). Salicylate induced tinnitus and altered the expression of the COX-2 and NR2B genes in the cochlea and midbrain of mice. These findings might contribute to further understanding of pathophysiology and therapy of tinnitus.