Effect of sodium nitroprusside on compound action potential thresholds in the gerbil cochlea.

The presence of active nitric oxide synthase (NOS) in the spiral ganglion cells of the cochlea suggests that the neuromodulator nitric oxide (NO) may play a role in hearing. This study investigated the effects of sodium nitroprusside (SNP), an NO donor, upon cochlear function mediated through its activation of guanylate cyclase. In gerbils, cochlear compound action potential (CAP) thresholds were recorded after cochlear perfusions of control and test solutions in four experimental groups. Perfusions were performed using the following: artificial perilymph solution (APS); the NO donor SNP; the guanylate cyclase inhibitor methylene blue (MB); and sodium dodecyl sulfate (SDS), which facilitates MB entrance into cells. SNP caused significant elevations of CAP thresholds from baseline (25 dB SPL +/- 1.54 dB to 64.3 dB SPL +/- 2.54 dB). SNP with MB also resulted in significant CAP threshold elevations (29.4 dB SPL +/- 4.27 dB to 38.1 dB SPL +/- 4.0 dB); however, these elevations were significantly lower than those seen in SNP perfusions without MB. Drilling perfusion holes and perfusion of APS, APS/SDS, and MB/SDS/APS solutions did not significantly affect CAP thresholds. These results suggest that the NO donor nitroprusside does affect cochlear neuromodulation and effects this mediation in part through NO activation of guanylate cyclase.