Downregulation of N-methyl-d-aspartate receptor 味1 subunit (GluN1) gene in inferior colliculus with aging

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• 作者：Yasunori Osumi^a ; Seiji Bruce Shibata^a ; Seiji Kanda^b ; ^c ; ^{kandas@takii.kmu.ac.jp} ; Masao Yagi^d ; Hisashi Ooka^b ; ^d ; Takashi Shimano^a ; Mikiya Asako^d ; Kohei Kawamoto^d ; Hiromichi Kuriyama^d ; Toshiya Inoue^d ; Toshimasa Nishiyama^c ; Toshio Yamashita^d ; Koichi Tomoda^d
• 关键词：NMDA ; N-methyl-d-aspartate ; GluN1 ; glutamate receptor ionotropic NMDA 味1 ; IC ; inferior colliculus ; ABRs ; auditory brain stem responses ; ISH ; in situ hybridization ; qPCR ; real-time PCR ; Gsn ; gelsolin
• 刊名：Brain Research
• 出版年：2012
• 期刊代码：8_00068993
• 类别：neu
• 出版时间：15 May, 2012
• 卷：1454
• 期：Complete
• 页码：23-32
• 文件大小：1081 K

摘要

Presbycusis is the impairment of auditory function associated with aging, which stems from peripheral cochlear lesions and degeneration of the central auditory process. The effect of age-induced peripheral hearing loss on the central auditory process is not fully understood. C57Bl/6 (C57) mice present accelerated peripheral hearing loss, which is well developed by middle-age and mimics the human presbycusis pattern. The aim of this study was to elucidate the molecular effects of peripheral hearing loss in the inferior colliculus (IC) with age between young and middle-aged C57 mice using cDNA microarray. Glutamate receptor ionotropic NMDA 味1 (GluN1) exhibited the greatest decrease in the middle-aged group as determined using cDNA microarray and by further assessment using real-time PCR (qPCR). Histological assessment with in situ hybridization of GluN1 showed significantly decreased expression in all IC subdivisions of the middle-aged group. GluN1 is a receptor for excitatory neurotransmission, and significant downregulation of this gene may be subsequent to the decline of afferent input from the cochlea in aging C57 mice. Consequently, using the combination of microarray, qPCR, and in situ hybridization, we showed that the decline of GluN1 in the IC of aging animals might have a key role in the pathogenesis of presbycusis.