Investigation On The Glu Receptor Mechanism Of The Spiral Ganglion Neuron Damage In Acoustic Trauma And The Interaction Between Glu And ATP Receptors

Evidences have shown that noise exposure causes damage to both hair cells and spiral ganglion neurons (SGN). The causes of degeneration and death of the SGN in acoustic trauma are as yet not completely known. It has been shown that glutamate and ATP are both important neurotransmitters in the hair cell/ afferent synapse, and also the Glu and ATP receptors co-exist in the membrane of the SGN. During the synaptic transmission, the inner hair cells release Glu and ATP into the synapse cleft,which activate their corresponding receptors in the SGN membrane. Both of Glu and ATP are involved in signal transduction and transmission of the cochlea. In this study, the possible Glu receptor mechanisms by which the SGN degenerate and die in acoustic trauma had been explored by using auditory electrophysiology, transmission electromicrology and whole-cell patch clamp recording. The interactions between Glu and ATP receptors were also addressed in the present study. Glu and its receptors played an important role in degeneration and death of SGN in acoustic trauma;ATP as an important neurotransmitter elicited an inward current of the SGN, which lead to the depolarization of the membrane of SGN and formation of auditory impulses. The pharmacological profile of ATP agonist and antagonist suggested the existence of P2X receptors in the SGN membrane. The inward currents elicited by ATP in isolated SGN were inhibited by the application of exogenous Glu, which could be blocked by the NMD A receptor antagonist, MK-801. These results suggest an interaction between Glu receptors and P2X receptors and NMDA receptors are mainly involved.