Recent advances in the development and function of type II spiral ganglion neurons in the mammalian inner ear

Zhang, Kaidi D.; Coate, Thomas M.

doi:10.1016/j.semcdb.2016.09.017

Cited by 42 publications

(38 citation statements)

References 95 publications

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“…fibers (Barclay et al 2011;Sundaresan et al 2016), to reach the mature configuration with each fiber exclusively innervating between 5 and 30 OHCs (Barclay et al 2011;Zhang and Coate 2017). This period of refinement is consistent with the reduction in the number of OHC synaptic ribbons that occurs from around P3 to the onset of hearing (Huang et al 2012).…”

Section: Morphological Changes During the Maturation Of Hair Cell Synsupporting

confidence: 68%

“…Over the years, several roles have been ascribed to type II SGNs (for a recent review, see Fuchs 2018). Based upon the current experimental data, the most likely function seems to be that they are activated solely by trauma (Flo-res et al 2015;Liu et al 2015; for a recent review, see Zhang and Coate 2017), leading to the assumption that they function as cochlear nociceptors (Weisz et al 2009;Liu et al 2015). OHC damage causes the release of ATP from nearby nonsensory cells, which strongly excites type II fibers (Liu et al 2015).…”

Section: Type II Spiral Ganglion Afferent Fibersmentioning

confidence: 99%

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Hair Cell Afferent Synapses: Function and Dysfunction

Johnson

Safieddine

Mustapha

et al. 2019

Cold Spring Harb Perspect Med

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To provide a meaningful representation of the auditory landscape, mammalian cochlear hair cells are optimized to detect sounds over an incredibly broad range of frequencies and intensities with unparalleled accuracy. This ability is largely conferred by specialized ribbon synapses that continuously transmit acoustic information with high fidelity and sub-millisecond precision to the afferent dendrites of the spiral ganglion neurons. To achieve this extraordinary task, ribbon synapses employ a unique combination of molecules and mechanisms that are tailored to sounds of different frequencies.Here we review the current understanding of how the hair cell's presynaptic machinery and its postsynaptic afferent connections are formed, how they mature, and how their function is adapted for an accurate perception of sound.

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Section: Morphological Changes During the Maturation Of Hair Cell Synsupporting

confidence: 68%

Section: Type II Spiral Ganglion Afferent Fibersmentioning

confidence: 99%

Hair Cell Afferent Synapses: Function and Dysfunction

Johnson

Safieddine

Mustapha

et al. 2019

Cold Spring Harb Perspect Med

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“…Type II SGNs selectively innervate the three rows of OHCs and extend a peripheral axon past the single row of IHCs that subsequently makes a 90°turn toward the cochlear base ( Fig. 1B) (Zhang and Coate, 2017). During outgrowth, Type II SGN peripheral axon turning occurs after the growth cone passes between the basolateral surfaces of cochlear-supporting cells.…”

Section: Resultsmentioning

confidence: 99%

Frizzled3andFrizzled6Cooperate withVangl2to Direct Cochlear Innervation by Type II Spiral Ganglion Neurons

Ghimire

Deans

2019

J. Neurosci.

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Type II spiral ganglion neurons provide afferent innervation to outer hair cells of the cochlea and are proposed to have nociceptive functions important for auditory function and homeostasis. These neurons are anatomically distinct from other classes of spiral ganglion neurons because they extend a peripheral axon beyond the inner hair cells that subsequently makes a distinct 90 degree turn toward the cochlear base. As a result, patterns of outer hair cell innervation are coordinated with the tonotopic organization of the cochlea. Previously, it was shown that peripheral axon turning is directed by a nonautonomous function of the core planar cell polarity (PCP) protein VANGL2. We demonstrate using mice of either sex that Fzd3 and Fzd6 similarly regulate axon turning, are functionally redundant with each other, and that Fzd3 genetically interacts with Vangl2 to guide this process. FZD3 and FZD6 proteins are asymmetrically distributed along the basolateral wall of cochlear-supporting cells, and are required to promote or maintain the asymmetric distribution of VANGL2 and CELSR1. These data indicate that intact PCP complexes formed between cochlear-supporting cells are required for the nonautonomous regulation of axon pathfinding. Consistent with this, in the absence of PCP signaling, peripheral axons turn randomly and often project toward the cochlear apex. Additional analyses of Porcn mutants in which WNT secretion is reduced suggest that noncanonical WNT signaling establishes or maintains PCP signaling in this context. A deeper understanding of these mechanisms is necessary for repairing auditory circuits following acoustic trauma or promoting cochlear reinnervation during regenerationbased deafness therapies.

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“…Ninety-five percent of all SGNs are type I SGNs, which innervate IHCs, are myelinated, and transmit the majority of all sound input (Dabdoub and Fritzsch, 2016;Meyer and Moser, 2010). The remaining 5% of SGNs are type II SGNs, which are unmyelinated and project past IHCs and pillar cells to form synapses with OHCs (Zhang and Coate, 2016). The type II SGNs are excitable in a glutamate-dependent manner (Weisz et al, 2009;Weisz et al, 2014) and capable of signaling to the brainstem following cochlear damage (Liu et al, 2015).…”

Section: Introductionmentioning

confidence: 99%