Abstract
Cochlear neurons are inevitably exposed to traumatic stress during surgical removal of an acoustic neuroma; that event is an important cause of postoperative cochlear neuronal degeneration, with subsequent loss of spiral ganglion cells (SGCs). The object of this study was to investigate whether preoperative pharmacological treatment can enhance the resistance of cochlear neurons to the traumatic stress of surgery. Cochlear neuronal degeneration was induced in 17 rats by controlled compression of the cerebellopontine angle portion of the cochlear nerve. Dizocilpine maleate (MK-801; 10 mg/kg), an N-methyl-D-aspartate (NMDA) antagonist, was administered intraperitoneally to six of the 17 rats 30 minutes before compression occurred. Two weeks after compression, each rat was killed, and the numbers of SGCs in histological preparations of temporal bones were counted. Spiral ganglion cells were more numerous in rats administered dizocilpine maleate (p < 0.03) than in rats that did not receive treatment, indicating that receptor-mediated glutamate neurotoxicity may participate in the pathogenesis of trauma-induced cochlear neuron death and that administration of an NMDA antagonist before surgery may protect the nerve from injury leading to hearing loss.
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