Olivocochlear neurons make temporary cholinergic synapses on inner hair cells of the rodent cochlea in the first two to three weeks after birth. Repetitive stimulation of these efferent neurons causes facilitation of evoked release and increased spontaneous release that continues for seconds to minutes. Presynaptic nAChRs are known to modulate neurotransmitter release from brain neurons. The present study explores the hypothesis that presynaptic nAChRs help to increase spontaneous release from efferent terminals on cochlear hair cells. Direct application of nicotine (which does not activate the hair cells' α9α10-containing nAChRs) produces sustained efferent transmitter release, implicating presynaptic nAChRs in this response. The effect of nicotine was reduced by application of ryanodine that reduces release of calcium from intra-terminal stores.

中文翻译：

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尼古丁诱发传出发射器释放到未成熟的耳蜗内毛细胞上。

在出生后的前两到三周，橄榄耳蜗神经元会在啮齿动物耳蜗的内毛细胞上产生临时的胆碱能突触。这些传出神经元的重复刺激导致诱发释放的促进和持续数秒至数分钟的自发释放增加。已知突触前 nAChR 可调节大脑神经元的神经递质释放。本研究探讨了突触前 nAChR 有助于增加耳蜗毛细胞传出末梢自发释放的假设。尼古丁的直接应用（不会激活毛细胞中含有 α9α10 的 nAChRs）会产生持续的传出递质释放，这表明突触前 nAChRs 参与了这种反应。