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Role of glutamate receptors in the spiral ganglion neuron damage induced by acoustic noise

Zhang Yanmin, Ma Bei, Gao Wenyuan, Wen Wen, Liu Haiying

Department of Physiology, the Second Military Medical University.Shanghai 200433

Abstract

The aim of the present study was to investigate the role of glutamate receptors in the damage of spiral ganglion neurons （SGNs） induced by acute acoustic noise. This investigation included in vivo and in vitro studies. In vivo, kynurenic acid （KYNA）, a broad-spectrum antagonist of glutamate receptors, was applied to the round window of guinea pigs, and its protective effect was observed. The animals were divided into three groups： control （saline, 0.9%, l0 #mu#L）, saline （0.9%, l0 #mu#L） + noise and KYNA （5 retool/L, l0 #mu#L） + noise. Saline and KYNA were applied to the round window membrane with a microsyringe. The animals were exposed to 110 dB SPL of white noise for 1 h. Hearing thresholds for auditory brainstem responses （ABRs） and compound action potentials （CAPs） in all animals were measured before and after treatment. The amplitudes of III waveform of ABR and NI waveform of CAP and the latency of NI waveform at different stimulation levels （intensity-amplitude and intensity-latency functions） were also measured. The cochleas were then dissected for transmission electron microscopy （TEM） after final electrophysiological measurement. In vitro, the SGNs of the normal guinea pigs were isolated and glutamate （100 #mu#mol/L or 1 000 #mu#mol/L） was added into the medium. The morphology of the SGNs was examined by light microscopy. In vivo results showed that the hearing function and morphology of the inner ear including hair cells and SGNs in the control group were normal. Compared with that in the control group the thresholds for ABR and CAP （click and tone burst） in saline + noise group were elevated significantly. The input-output functions showed that the amplitudes of Ⅲ waveform of ABR and N1 waveform of CAP decreased and the latency of N1 waveform increased obviously. There was significant difference in the amplitude and latency between saline + noise group and KYNA + noise group （P〈0.05）. TEM indicated obvious swelling and vacuoles at the terminate of dendrites of SGNs in NS + noise group. On the contrary, the afferent dendrites in KYNA + noise group showed normal appearance without swelling and vacuoles. In vitro experiment showed that the isolated SGNs of guinea pigs obviously swelled and even died after application of 100 #mu#mol/L or 1 000 #mu#mol/L glutamate. These results suggest that noise exposure causes hearing impairment, damage of hair cells and hair cell/afferent synapse and death of SGNs. The antagonist of glutamate receptors provides protective effects against hearing loss and SGN damage. It is inferred that excessive release of glutamate from the inner hair cells induced by noise may be responsible for these damages. Glutamate receptors are involved in the degeneration and death of SGNs.

Key words: spiral ganglion neuron;heating loss;Glutamate;glutamate receptors;kynurenic acid

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Citing This Article：

Zhang Yanmin, Ma Bei, Gao Wenyuan, Wen Wen, Liu Haiying. Role of glutamate receptors in the spiral ganglion neuron damage induced by acoustic noise. Acta Physiol Sin 2007; 59 (1): 103-110 (in Chinese with English abstract).