Nitric oxide in glutamate-induced compound action potential threshold shifts.

Objective: Investigate the role of NO as a neurotransmitter in the gerbil cochlea and the effects of (7-NI) on compound action potential (CAP) threshold elevations induced by l-glutamate, an agonist at the NMDA glutamate receptor subtype, to further elucidate the role of NO in cochlear excitotoxicity.

Method: In anesthetized gerbils, CAP thresholds were recorded before and after cochlear perfusions with a control solution of artificial perilymph (APS) and a test solution of L-glutamate (GA) in three experimental groups.

Results: The control group showed no CAP threshold elevations (p<0.05) when APS was perfused after systemic pre-treatment with 7-NI. GA perfusion alone caused significant elevation (p<0.05) of the mean cochlear CAP threshold (25 dB SPL+/-5.8 dB to 78 dB SPL+/-19.5 dB). The CAP threshold elevation was prevented (p<0.05) when the animals were pretreated with 7-NI before GA perfusion (24 dB SPL+/-4.2dB to 27 dB SPL+/-6.7 dB).

Conclusion: NO mediates excitotoxicity when the cochlea is perfused with L-glutamate.