Abstract: Objective To observe the damage of the afferent nerve endings underlying cochlear Inner Hair Cells (IHCs) caused by noise exposure, and to explore the injury mechanism of the above lesion with respect to the excitotoxicity of the excessive afferent neurotransmitter glutamate in cochlea. Methods Thirty-eight guinea pigs served as subjects. The animals were randomly distributed into 5 groups: a normal control group, and 4 experimental groups including the group of 8 hours, 1 day, 3 days and 7 days after noise exposure. The 4 experimental groups were immersed in the noise of 120 dB L_p, 1/3 octave 4 kHz narrow band noise for 4 h. The altitude of Cochlea Microphonics (CM) and the response threshold of Compound Action Potential (CAP) in the left ear of animals were measured. Ultrathin sections (70 nm) were cut from the Corti organs of the animals' left ear. The ultrastructural changes of cochlea and the densities of glutamateimmunogold particle in IHCs and Outer Hair Cells (OHCs) were observed under the transmission electron microscope. Results In the four experimental groups, the non-linear property of CM lessened and the threshold of CAP enhanced, and vacuolizations appeared in the cell plasma of OHCs and in the afferent nerve endings underneath IHCs. Compared with that of the normal control group, the immunogold particle densities of IHCs in the left ear reduced significantly at the group of 8 hours after noise exposure, but there were no significant difference in the group of 1 day, 3 days and 7 days after noise exposure respectively. Conclusion (1) The damaged portion of cochlea caused by noise exposure not only involves OHCs, but also the afferent nerve endings underneath IHCs; (2) The afferent neurotransmitter glutamate in IHCs can be over-released after noise exposure, and the excitotoxicity of the excessive glutamate may be one of the injury mechanisms for the lesion of afferent nerve endings underlying IHCs caused by noise exposure.