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首页> 外文期刊>The European Journal of Neuroscience >Dopamine inhibition of auditory nerve activity in the adult mammalian cochlea.
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Dopamine inhibition of auditory nerve activity in the adult mammalian cochlea.

机译：多巴胺抑制成年哺乳动物耳蜗的听觉神经活动。

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摘要

Efferent feedback systems provide a means for modulating the input to the central nervous system. The lateral olivocochlear efferents modulate auditory nerve activity via synapses with afferent dendrites below sensory inner hair cells. We examined the effects of dopamine, one of the lateral olivocochlear neurotransmitters, by recording compound and single unit activity from the auditory nerve in adult guinea pigs. Intracochlear application of dopamine reduced the compound action potential (CAP) of the auditory nerve, increased the thresholds and decreased the spontaneous and driven discharge rates of the single unit fibres without changing their frequency-tuning properties. Surprisingly, dopamine antagonists SCH-23390 and eticlopride decreased CAP amplitude as did dopamine. In some units, both SCH-23390 and eticlopride increased the basal activity of auditory nerve fibres leading to an improvement of threshold sensitivity and a decrease of the maximum driven discharge rates to sound. In other units, the increase in firing rate was immediately followed by a marked reduction to values below predrug rates. Because CAP reflects the summed activity of auditory nerve fibres discharging in synchrony, both the decrease in sound-driven discharge rate and the postexcitatory reduction account for the reduction in CAP. Ultrastructural examination of the cochleas perfused with eticlopride showed that some of the afferent dendrites were swollen, suggesting that the marked reduction in firing rate may reflect early signs of excitotoxicity. Results suggest that dopamine may exert a tonic inhibition of the auditory nerve activity. Removal of this tonic inhibition results in the development of early signs of excitotoxicity.
机译：传出的反馈系统提供了一种调节中枢神经系统输入的方法。侧耳小耳出射通过与感觉内部毛细胞下方的传入树突的突触来调节听觉神经活动。我们通过记录成年豚鼠听神经的化合物和单个单位的活性，检查了多巴胺（一种侧耳蜗神经递质）的作用。耳蜗内应用多巴胺可降低听觉神经的复合动作电位（CAP），提高阈值并降低单根纤维的自发和驱动放电速率，而不会改变它们的频率调谐特性。出人意料的是，多巴胺拮抗剂SCH-23390和艾替洛必利与多巴胺一样降低CAP幅度。在某些单位中，SCH-23390和艾替洛必利均增加了听神经纤维的基础活性，从而导致阈值灵敏度的提高和声音最大驱动放电率的降低。在其他单位中，射击速率增加后立即显着降低到低于前药速率的值。因为CAP反映了同步发出的听觉神经纤维的总活动，所以声音驱动的放电速率的降低和兴奋后的减少均导致CAP的降低。对充有艾替洛必利的耳蜗进行超微结构检查，结果显示一些传入的树突肿胀，表明放电速率的明显降低可能反映了兴奋性毒性的早期迹象。结果表明，多巴胺可能对听神经活动产生强直抑制作用。消除这种强直抑制作用会导致兴奋性毒性的早期迹象的发展。

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