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Published on: November 26, 2015
Nimodipine ameliorates trauma-induced cochlear neuronal death
Tetsuji Sekiya1, Akinori Yagihashi, Kenichiro Asano
1Department of Neurosurgery, Hirosaki University School of Medicine, 5 Zaifu-cho, Hirosaki, 036-8216, Japan. seky@cc.hirosaki-u.ac.jp
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.
Insights
Nimodipine, an L-type calcium channel blocker, protected cochlear neurons from injury-induced death in rats. This finding suggests nimodipine may improve hearing preservation during surgeries near the cochlear nerve.
Area of Science:
- Neuroscience
- Otolaryngology
- Pharmacology
Background:
- Excessive intracellular calcium (Ca2+) influx into injured cochlear neurons triggers cell death pathways.
- Calcium-activated enzymes contribute to spiral ganglion neuron degeneration after injury.
- Calcium channel antagonists are potential therapeutic agents to prevent neuronal loss.
Purpose of the Study:
- To investigate the neuroprotective potential of nimodipine, an L-type calcium channel blocker, against cochlear nerve injury.
- To evaluate the efficacy of nimodipine in preventing spiral ganglion cell death following surgical trauma.
Main Methods:
- Rats (n=6) received pre-operative nimodipine treatment for one week.
- A quantitative compression injury was applied to the cerebellopontine angle portion of the cochlear nerve.
- Post-operative nimodipine treatment was administered for 10 days, followed by histological examination of temporal bones.
Main Results:
- Histological analysis revealed statistically significant rescue of spiral ganglion cells in the basal turn of the cochlea.
- The protective effect was observed in the group treated with nimodipine following compression injury.
- The basal turn experienced the least traumatic impact in this experimental setup.
Conclusions:
- Nimodipine demonstrates neuroprotective effects against cochlear nerve injury.
- Nimodipine may serve as a valuable adjunct for intra- and post-operative hearing preservation.
- This suggests potential benefits in surgeries like vestibular schwannoma excision.
