谷氨酸对豚鼠畸变产物耳声发射和听性脑干反应的影响

目的 研究外源性谷氨酸对畸变产物耳声发射(distortion product otoacoustlcemission，DPOAE)、听性脑干反应(auditory brainstem response，ABR)及耳蜗形态学的影响。方法应用豚鼠全耳蜗灌流技术，耳蜗灌流10mmol/L谷氨酸2h，分别记录灌流前、后DPOAE和ABR；耳蜗微音电位(cochlear microphonics，CM)和听神经复合动作电位(compound action potential，CAP)；应用透射电镜进行耳蜗形态学观察。结果灌流人工外淋巴液前、后CM及CAP无改变；灌流10mmol／L谷氨酸后DPOAE无改变，ABR潜伏期延长；同样灌流10mmol／L谷氨酸后CM幅度虽有下降、但是其非线性特点无改变；CAP阈值平均升高了35dB；灌流谷氨酸后内毛细胞及其下方神经纤维出现空泡。结论谷氨酸作为耳蜗主要的兴奋性传入神经递质，过度释放可以产生兴奋性毒性，损伤耳蜗内毛细胞及传入神经。同时本实验为建立听神经病的动物模型提供了一个参考方法。

Effect of glutamate on distortion product otoacoustic emission and auditory brainstem response in guinea pigs

Objective To investigate the changes of the potentials and structure of the guinea pig cochlear during whole cochlear perfusion with glutamate. Methods Cochlear microphonics(CM),compound action potential(CAP), distortion product otoacoustic emission(DPOAE)and auditory brainstem response(ABR)were measured to indicate the cochlear functional properties during whole cochlear perfusion. The morphology of the cochlear was monitored by transmission electron microscopy. Results There were no significant DPOAE changes before and after glutamate perfusion. CM I/O function maintained a nonlinear characteristic during infusion. After glutamate perfusion, ABR latencies were delayed. There was significant difference in CAP threshold before and after glutamate perfusion. The average CAP threshold was elevated 35 dB. The OHCs appeared normal, but IHCs and afferent dendrites showed cytoplasmic blebs after glutamate infusion. Conclusions Glutamate is thought to be a primary amino acid neurotransmitter at the synapses formed by cochlear hair cells and spiral ganglion neurons. However, the excessive glutamate is neurotoxic for cells, and it can destroy the IHCs and spiral ganglion neurons. The present method can also be built up as an animal model of auditory neuropathy.