NMDA Receptor Blockage Protects Against Permanent Noise-Induced Hearing Loss but Not Its Potentiation by Carbon Monoxide
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2001/04/01
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Description:While a clear role has been proposed for glutamate as a putative neurotransmitter at the inner hair cell type I spiral ganglion cell synapse, the possible role of excessive glutamate release in cochlear impairment and of NMDA receptors in such a process is uncertain. The present study compares the protective effects of (+)-MK-801, an NMDA receptor antagonist, and the relatively inactive isomer (-)-MK-801 against permanent noise-induced hearing loss (NIHL). The study also asks whether (+)-MK-801 can protect against the NIHL potentiation by carbon monoxide (CO). Rats (n = 6) were exposed to 100-dB, 13.6-kHz octave-band noise for 2 h after receiving injection of (+)-MK-801 hydrogen maleate (1 mg/kg), (-)-MK-801 hydrogen maleate (1 mg/kg), or saline. Other groups of animals were exposed to the combination of noise and CO (1200 ppm) after receiving (+)-MK-801 or saline. Additional subjects received (+)-MK-801, saline or CO exposure alone. Compound action potential (CAP) threshold sensitivities were compared 4 weeks after the exposures. The results show significant protection by (+)-MK-801 against the permanent CAP threshold elevation induced by noise alone, but no protective effect of (-)-MK-801. (+)-MK-801 produced limited protection against threshold shifts induced by the combination of noise and CO. Outer hair cell (OHC) loss was not protected by (+)-MK-801 administration. The data suggest that NMDA receptor stimulation may play a role in NIHL resulting from fairly mild noise exposure. The data do not support a role for NMDA receptor stimulation in the potentiation of NIHL that results from simultaneous exposure to CO and noise. [Description provided by NIOSH]
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ISSN:0378-5955
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Pages in Document:108-115
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Volume:154
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Issue:1
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NIOSHTIC Number:nn:20029663
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Citation:Hear Res 2001 Apr; 154(1-2):108-115
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Contact Point Address:University of Oklahoma, Health Sciences Center, College of Pharmacy, Oklahoma City 73190
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Email:guangdi-chen@ouhsc.edu
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Federal Fiscal Year:2001
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Performing Organization:University of Oklahoma, Health Sciences Center, Oklahoma Center for Toxicology, Oklahoma City, Oklahoma
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Peer Reviewed:True
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Start Date:19970901
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Source Full Name:Hearing Research
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End Date:20000831
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Main Document Checksum:urn:sha-512:a058e9e5c3a795a9b926c14270dc428d499d127c3e01290ff53a3a132d99cfa67253b496f963e4e43e02854c85a7da459d2b8e1332d9e448d9be670d58c44409
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