Puel J L, Saffiedine S, Gervais d'Aldin C, Eybalin M, Pujol R
INSERM U. 254, Université de Montpellier-I, France.
C R Acad Sci III. 1995 Jan;318(1):67-75.
Cochlear ischemia and acoustic trauma result in an immediate hearing loss accompanied by the complete disruption of the terminal dendrites of primary auditory neurons postsynaptic to the sensory inner hair cells (IHCs). This synaptic uncoupling, due to an acute glutamate (IHC neurotransmitter) excitotoxicity process, can be mimicked by glutamate agonists. Thus, we have followed over a 5-day period the responses of guinea-pig cochleas to a local application of 200 microM AMPA. This application immediately results in a destruction of all postsynaptic endings of the auditory nerve, resulting in a total loss of cochlear potentials. Twenty-four hours after this excitotoxic injury, the inner hair cells were contacted by repaired postsynaptic dendrites and the cochlear potential had partially recovered. This process of neo-synaptogenesis was completed and the potentials were fully restored at 5 days post exposure. As shown by in situ hybridization, an up-regulation of NMDA and metabotropic glutamate receptors in the primary auditory neurons occurred during this process of recovery. This process of neo-synaptogenesis and functional recovery probably accounts for restoring hearing after temporary losses due to excitotoxic-related pathologies.
耳蜗缺血和声学创伤会导致立即性听力丧失，并伴有感觉性内毛细胞（IHC）突触后初级听觉神经元终末树突的完全破坏。这种由于急性谷氨酸（IHC神经递质）兴奋性毒性过程导致的突触解偶联，可被谷氨酸激动剂模拟。因此，我们在5天的时间里追踪了豚鼠耳蜗对局部应用200微摩尔AMPA的反应。这种应用立即导致听神经所有突触后末梢的破坏，导致耳蜗电位完全丧失。在这种兴奋性毒性损伤24小时后，修复后的突触后树突与内毛细胞接触，耳蜗电位部分恢复。新突触形成过程在暴露后5天完成，电位完全恢复。原位杂交显示，在这个恢复过程中，初级听觉神经元中的NMDA和代谢型谷氨酸受体上调。这种新突触形成和功能恢复过程可能是因兴奋性毒性相关病理导致的暂时性听力丧失后恢复听力的原因。
