Reijntjes Daniël O J, Pyott Sonja J
Department of Otorhinolaryngology/Head and Neck Surgery, University Medical Center Groningen, Groningen, The Netherlands.
Department of Otorhinolaryngology/Head and Neck Surgery, University Medical Center Groningen, Groningen, The Netherlands.
Hear Res. 2016 Jun;336:1-16. doi: 10.1016/j.heares.2016.03.011. Epub 2016 Mar 25.
The spiral ganglion neurons (SGNs) are the first action potential generating neurons in the auditory pathway. The type I SGNs contact the sensory inner hair cells via their peripheral dendrites and relay auditory information to the brainstem via their central axon fibers. Individual afferent fibers show differences in response properties that are essential for normal hearing. The mechanisms that give rise to the heterogeneity of afferent responses are very poorly understood but are likely already in place at the peripheral dendrites where synapses are formed and action potentials are generated. To identify these molecular mechanisms, this review synthesizes a variety of literature and comprehensively outlines the cellular and molecular components positioned to regulate SGN afferent dendrite excitability, especially following glutamate release. These components include 1) proteins of the SGN postsynapses and neighboring supporting cells that together shape glutamatergic signaling, 2) the ion channels and transporters that determine the intrinsic excitability of the SGN afferent dendrites, and 3) the neurotransmitter receptors that extrinsically modify this excitability via synaptic input from the lateral olivocochlear efferents. This cellular and molecular machinery, together with presynaptic specializations of the inner hair cells, can be collectively referred to as the type I afferent signaling complex. As this review underscores, interactions of this signaling complex determine excitability of the SGN afferent dendrites and the afferent fiber responses. Moreover, this complex establishes the environmental milieu critical for the development and maintenance of the SGN afferent dendrites and synapses. Motivated by these important functions, this review also indicates areas of future research to elucidate the contributions of the afferent signaling complex to both normal hearing and also hearing loss.
螺旋神经节神经元（SGNs）是听觉通路中首个产生动作电位的神经元。I型SGNs通过其外周树突与感觉性内毛细胞接触，并通过其中枢轴突纤维将听觉信息传递至脑干。单个传入纤维在反应特性上存在差异，这对正常听力至关重要。引发传入反应异质性的机制目前了解甚少，但可能在形成突触并产生动作电位的外周树突中就已存在。为了确定这些分子机制，本综述综合了各种文献，并全面概述了用于调节SGN传入树突兴奋性的细胞和分子成分，尤其是在谷氨酸释放之后。这些成分包括：1）SGN突触后和相邻支持细胞的蛋白质，它们共同塑造谷氨酸能信号传导；2）决定SGN传入树突内在兴奋性的离子通道和转运体；3）通过外侧橄榄耳蜗传出纤维的突触输入从外部改变这种兴奋性的神经递质受体。这种细胞和分子机制，连同内毛细胞的突触前特化，可统称为I型传入信号复合体。正如本综述所强调的，这种信号复合体的相互作用决定了SGN传入树突的兴奋性和传入纤维反应。此外，这种复合体建立了对SGN传入树突和突触的发育与维持至关重要的环境。受这些重要功能的驱动，本综述还指出了未来研究的领域，以阐明传入信号复合体对正常听力和听力损失的贡献。
