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

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Patel, MR; Stamat, JC; Zdanski, CJ; Ebert, CS; Prazma, J

Published Date

  • May 2008

Published In

Volume / Issue

  • 239 / 1-2

Start / End Page

  • 54 - 59

PubMed ID

  • 18434048

Pubmed Central ID

  • 18434048

International Standard Serial Number (ISSN)

  • 0378-5955

Digital Object Identifier (DOI)

  • 10.1016/j.heares.2008.01.007

Language

  • eng

Conference Location

  • Netherlands