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Titolo:
Effects of kynurenic acid as a glutamate receptor antagonist in the guineapig
Autore:
Khan, MJ; Seidman, MD; Quirk, WS; Shivapuja, BG;
Indirizzi:
Henry Ford Hosp, Dept Otorhinolaryngol Head & Neck Surg, Detroit, MI 48202USA Henry Ford Hosp Detroit MI USA 48202 ad & Neck Surg, Detroit, MI 48202USA Minnesota State Univ, Dept Commun Disorders, Man Kato, MN 56002 USA Minnesota State Univ Man Kato MN USA 56002 orders, Man Kato, MN 56002 USA
Titolo Testata:
EUROPEAN ARCHIVES OF OTO-RHINO-LARYNGOLOGY
fascicolo: 4, volume: 257, anno: 2000,
pagine: 177 - 181
SICI:
0937-4477(200004)257:4<177:EOKAAA>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
METHYL-D-ASPARTATE; XENOPUS-LAEVIS; LATERAL-LINE; COCHLEA; NEUROTRANSMISSION; DISORDERS; AGONISTS; THERAPY; ORGAN;
Keywords:
glutamate excitotoxicity; noise-induced hearing loss; kynurenic acid; noise attenuation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Seidman, MD Henry Ford Hosp, Dept Otorhinolaryngol Head & Neck Surg, 2799 W Grand Blvd, Detroit, MI 48202 USA Henry Ford Hosp 2799 W Grand Blvd Detroit MI USA 48202 202 USA
Citazione:
M.J. Khan et al., "Effects of kynurenic acid as a glutamate receptor antagonist in the guineapig", EUR ARCH OT, 257(4), 2000, pp. 177-181

Abstract

Glutamate excitotoxicity is implicated in both the genesis of neural injury and noise-induced hearing loss (NIHL). Acoustic overstimulation may result in excessive synaptic glutamate, resulting in excessive binding to post-synaptic receptors and the initiation of a destructive cascade of cellular events, thus leading to neuronal degeneration and NIHL. The purpose of this study was to determine whether this apparent excitotoxicity can be attenuated by kynurenic acid (KYNA), a broad-spectrum glutamate receptor antagonist, and protect against noise-induced temporary threshold shifts (TTS). Guinea pigs were randomly assigned to three separate groups. Baseline compound action potentials (CAP) thresholds and cochlear microphonics (CM) were recorded. Group I was treated with physiologic saline as a vehicle control applied to the round window membrane that was followed by 110 dB SPL wide-band noise for 90 min. Group II received 5 mM KYNA followed by noise exposure, and group III received 5 mM KYNA alone without noise exposure. Post-drug and noise levels of CAP thresholds and CM were then obtained. Noise exposure inthe control group caused a significant temporary threshold shift (TTS) of 30-40 dB across the frequencies tested (from 3 kHz to 18 kHz). Animals thatreceived 5 mM KYNA prior to noise exposure (group II) showed statisticallysignificant protection against noise-induced damage and demonstrated a minimal TTS ranging between 5 and 10 dB at the same frequencies. Animals in group III receiving KYNA without noise exposure showed no change in thresholds. Additionally, cochlear microphonics showed no considerable difference inthreshold shifts when controls were compared to KYNA-treated animals. These re suits show that antagonizing glutamate receptors can attenuate noise-induced TTS, suggesting that glutamate excitotoxicity may play a role in acoustic trauma.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 10:06:58