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cept of tinnitus. Age-related differences in subunit plasticity associated with noise-exposure might provi- de insights into the increased incidence of tinnitus in the elderly (Supported in part by American Tinnitus Association, NIH DC00151, and Merck Inc.).

Hypoxic changes of central nervous system in noise-exposed mouse. (Abstract of ARO Meeting Denver, Colorado) Young-Jin Kim1, Hun Hee Kang2, Joong Ho Ahn2, Kwang-Sun Lee2, Jong Woo Chung2 1Daejin medical center, 2Asan medical center

Background and objectives: When noise-induced hearing loss occurs, hypoxia is detected in inner ear tissues. In previous study noise-induced inner ear hypoxia was proved by the increase of HIF-1a, which is expressed? in the nucleus under hypoxic condition. Another hypoxic marker, pimonidazole is also widely used to see the hypoxic area by injection from outside. Existence of tinnitus or hyperacusis with noise-induced hearing change may suggest the change of central nervous system, but no exact site or ti- ming of change is alleged until now. The study is designed to investigate the sitespecific hypoxic change in central auditory pathway during noise induced threshold shift. Materials and Methods: Fifty six BALB/c hybrid mice with normal hearing were exposed to 120 dB SPL broad band noise for 3 hours. Immediately after noise and 7 days after noise exposure, the brains of mice were extracted. They were cryosectioned by 15 (m thickness and examined by immunofluore- scence using monoclonal antibody of HIF-1a and pimonidazole HCL (hypoxyprobe(-1). Result: After noise, the hearing thresholds of mice decreased to 49.5 ( 8.0 dB HL and the hearing were recovered to 27.9 ( 4.3 dB HL in 7 days. In the coronal section of brain, HIF-1a was detected immedi- ately after noise in the auditory cortex, hippocampus and inferior colliculus. At least for 7 days, these signals persisted although without additional noise exposure. When the same slides were double stained by hypoxyprobe(-1, auditory cortex, hippocampus and inferior colliculus showed more localized hypoxic signals. The uptake of pimonidazole increased after 7 days. Conclusion: In noise-induced transient threshold shift, hypoxia occurred in central nervous system and it persisted until 7 days, even though hearing was recovered. These changes were sensitive in auditory cortex and hippocampus. Key words: Noise-induced hearing loss, Central nervous system, Hypoxia, Hypoxia-inducible factor 1a, Pimonidazole

Molecular Correlates of Noise-Induced Tinnitus:Alterations in Gene Expression Influen- cing Inhibition in the Dorsal Cochlear Nucleus. (Abstract of ARO Meeting Denver, Colorado) Avril Genene Holt1, Catherine Lomax2, Susan Land1, James Kaltenbach1 1Wayne State University, 2University of Michigan

Noise-induced tinnitus can be a debilitating condition that decreases quality of life. A hallmark of noise- induced central tinnitus is thought to be a change in the balance between inhibition and excitation with sustained increases in spontaneous neuronal activity that begin in the dorsal cochlear nucleus (DCN). To explore mechanisms involved in this imbalance we screened nine genes influencing inhibitory neuro- transmission in the DCN for changes in expression at different times following noise exposure. Animals were divided into ten groups: half were exposed to an intense (125-130 dB SPL) 10 kHz tone for 4 hours, and half were age matched unexposed controls. Exposed animals were assessed at each of 5 different post-exposure recovery times: 0d, 2d, 5d, 14d and 29 days. The expression of nine genes, four glycine receptor genes (glyR1a, glyR2a, glyR3a, glyRb), four muscarinic receptors (muscR2, muscR3, muscR4, muscR5), and ChaT were assessed across groups. Each experimental group consisted of 3 RNA pools for each time-point, comprised of the DCN from three rats. Real time RT-PCR indicates that the DCN has

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