Hakuba N, Koga K, Gyo K, Usami S I, Tanaka K
Department of Otolaryngology, Ehime University School of Medicine, Ehime 791-0295, Japan.
J Neurosci. 2000 Dec 1;20(23):8750-3. doi: 10.1523/JNEUROSCI.20-23-08750.2000.
Acoustic overstimulation is one of the major causes of hearing loss. Glutamate is the most likely candidate neurotransmitter for afferent synapses in the peripheral auditory system, so it was proposed that glutamate excitotoxicity may be involved in noise trauma. However, there has been no direct evidence that noise trauma is caused by excessive release of glutamate from the inner hair cells (IHCs) during sound exposure because studies have been hampered by powerful glutamate uptake systems in the cochlea. GLAST is a glutamate transporter highly expressed in the cochlea. Here we show that after acoustic overstimulation, GLAST-deficient mice show increased accumulation of glutamate in perilymphs, resulting in exacerbation of hearing loss. These results suggest that GLAST plays an important role in keeping the concentration of glutamate in the perilymph at a nontoxic level during acoustic overstimulation. These findings also provide further support for the hypothesis that IHCs use glutamate as a neurotransmitter.
听觉过度刺激是听力损失的主要原因之一。谷氨酸是外周听觉系统传入突触最有可能的候选神经递质,因此有人提出谷氨酸兴奋性毒性可能与噪声性损伤有关。然而,目前尚无直接证据表明噪声性损伤是由声音暴露期间内毛细胞(IHC)过度释放谷氨酸所致,因为耳蜗中强大的谷氨酸摄取系统阻碍了相关研究。GLAST是一种在耳蜗中高度表达的谷氨酸转运体。在此我们表明,听觉过度刺激后,缺乏GLAST的小鼠外淋巴中谷氨酸积累增加,导致听力损失加剧。这些结果表明,GLAST在听觉过度刺激期间将外淋巴中谷氨酸浓度维持在无毒水平方面发挥着重要作用。这些发现也为IHC使用谷氨酸作为神经递质这一假说提供了进一步支持。