Molecular basis for ischemic cochlear dysfunction

1995 Fiscal Year Final Research Report Summary

• Project/Area Number: 06671716
• Research Category: Grant-in-Aid for General Scientific Research (C)
• Allocation Type: Single-year Grants
• Research Field: Otorhinolaryngology
• Research Institution: Osaka University
• Principal Investigator: KAWASAKI Yosiaki Osaka University Otolaryngology Assistant Professor, 医学部, 講師 (00224767)
• Co-Investigator(Kenkyū-buntansha): KAWAI Kensuke Teikyo University Neurosurgery Research assistant, 医学部, 助手 (70260924) ; DOI Katsumi Osaka University Otolaryngology Assistant Professor, 医学部, 講師 (40243224)
• Project Period (FY): 1994 – 1995
• Keywords: Cochlea / Ischemia / Sensorin ral / Hearing loss / Glutamate receptor / Microtubule-related protein / Up-regulation

Research Abstract

To determine the molecular basis for the cause of sensorineural hearing loss due to ischemic cochlear dysfunction, we developed ischemic model animals by using Korpatchev's method. Total RNA was extracted from the cochlea of the normal and ischemic model animals. cDNAs were prepared for the PCR analysis, and the specific primers for glutamate receptor gene family (GluR), and microtubule-associated proteins (Map2) were synthesized and used to amplify those molecules from the normal and ischemic cochleae.
From the ischemic cochleae, all of the eight sununits of GluR1-4 were detected by the PCR analysis. The expression of GluR2 subunit was up-regulated in the ischemic cochlea, compared to that of the normal cochlea. The expression of Map2c was also up-regulated in the ischemic cochlea. These results suggest that sensorinueral hearing loss due to ischemic cochlea dysfunction must be related to the molecular changes in the cytoskeletal protein of hair cells as well as in the receptor channels for the afferent synapses between the hair cells and the spiral ganglion cells.