title: Nimodipine ameliorates trauma-induced cochlear neuronal death.
abstract: Excessive entry of Ca2+ into injured cochlear neurons activates various Ca(2+)-activated enzymes and subsequent spiral ganglion cell death. Therefore, preventing intracellular calcium overload by using Ca2+ channel antagonists may become an important countermeasure to spiral ganglion cell death. We experimentally investigated whether an L-type Ca2+ channel blocker (nimodipine) can rescue traumatized cochlear neurons from degeneration. A group of rats (n = 6) was pre-operatively treated with nimodipine for one week and compression injury was applied to the cerebellopontine angle portion of the cochlear nerve in a highly quantitative fashion. The rats from the compression with nimodipine treatment groups were post-operatively treated with nimodipine for 10 days and killed for histological examination. The histological analysis of the temporal bones revealed that the spiral ganglion cells in the basal turn of the cochlea where the magnitude of traumatic impact had been the least in our experimental condition were rescued in a statistically significant fashion in the compression with nimodipine treatment group. The results of the present study indicate that nimodipine may become an intra- and post-operative important adjunct to raise the rate of hearing preservation in vestibular schwannoma excision or other cerebellopontine angle surgical interventions.
authors.affiliation: Department of Neurosurgery, Hirosaki University School of Medicine, 5 Zaifu-cho, Hirosaki, 036-8216, Japan. seky@cc.hirosaki-u.ac.jp
authors.forename: Tetsuji
authors.initials: T
authors.lastname: Sekiya
authors.forename: Akinori
authors.initials: A
authors.lastname: Yagihashi
authors.forename: Kenichiro
authors.initials: K
authors.lastname: Asano
authors.forename: Shigeharu
authors.initials: S
authors.lastname: Suzuki
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology* / Q000627:therapeutic use; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology; D016923:Cell Death / Q000187:drug effects / Q000502:physiology; D003056:Cochlear Nerve / Q000187:drug effects* / Q000293:injuries* / Q000503:physiopathology; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D008297:Male; D009409:Nerve Crush; D009410:Nerve Degeneration / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D009464:Neuroma, Acoustic / Q000601:surgery; D009475:Neurons, Afferent / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D019635:Neurosurgical Procedures / Q000009:adverse effects; D009553:Nimodipine / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D013136:Spiral Ganglion / Q000473:pathology / Q000503:physiopathology*; D013314:Stress, Mechanical; D000160:Vestibulocochlear Nerve Diseases / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology
chemical_list: D002121:Calcium Channel Blockers; D009553:Nimodipine; D002118:Calcium