Nitric oxide in glutamate-induced compound action potential threshold shifts

作者：Patel Mihir R; Stamat Jocelyn C; Zdanski Carlton J^*; Ebert Charles S Jr; Prazma Jiri

来源：Hearing Research, 2008, 239(1-2): 54-59.

DOI：10.1016/j.heares.2008.01.007

• cochlea
• excitatory amino acids
• glutamate
• nitric oxide
• 7-nitroindazole
• excitotoxicity

Objective: Investigate the role of NO as a neuro transmitter 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 +/- 4.2 dB to 27 dB SPL +/- 6.7 dB).
Conclusion: NO mediates excitotoxicity when the cochlea is perfused with L-glutamate.

• 出版日期2008-5
• 单位西北大学