Postsynaptic Targets of Type II Auditory Nerve Fibers in the Cochlear Nucleus.

Benson, Thane E.; Brown, M. Christian

doi:10.1007/s10162-003-4012-3

Cited by 40 publications

(37 citation statements)

References 63 publications

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“…The labelling of Wbres in the AVCN, DCN, superWcial granule cell layer and granule cell lamina (as noted above) likely arise from the cochlear SGNII (Berglund and Ryugo 1987;Brown et al 1988;Brown and Ledwith 1990;Ryugo et al 1991;Berglund and Brown 1994;Hurd et al 1999;Benson and Brown 2004). SGNII, with cell bodies located within Rosenthal's canal in the cochlea, are known to express peripherin in both rat (HaWdi 1998) and mouse (Schimmang et al 2003).…”

Section: Discussionmentioning

confidence: 94%

“…SpeciWcally, these Wbres most likely arise from the unmyelinated cochlear type II spiral ganglion neurons (SGNII) (Berglund and Ryugo 1987;Ryugo et al 1991), which express peripherin (HaWdi 1998), innervate the AVCN and the DCN, but not the PVCN (Brown et al 1988) and make up less than 10% of the primary auditory neuronal population. Peripherin expressing Wbres observed innervating the superWcial granule cell layer and the granule cell lamina are also most likely SGNII axons, which are well known to have terminations within these regions and where postsynaptic targets of SGNII have been determined (Brown and Ledwith 1990;Berglund and Brown 1994;Hurd et al 1999;Benson and Brown 2004).…”

Section: Cerebellummentioning

confidence: 98%

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Neuronal expression of peripherin, a type III intermediate filament protein, in the mouse hindbrain

Barclay

Noakes

Ryan

et al. 2007

Histochem Cell Biol

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Peripherin is a 57 kDa Type III intermediate filament protein associated with neurite extension, neuropathies such as amyotrophic lateral sclerosis, and cranial nerve and dorsal root projections. However, knowledge of peripherin expression in the CNS is limited. We have used immunoperoxidase histochemistry to characterise peripherin expression in the mouse hindbrain, including the inferior colliculus, pons, medulla and cerebellum. Peripherin immunolabelling was observed in the nerve fibres and nuclei that are associated with all cranial nerves [(CN) V-XII] in the hindbrain. Peripherin expression was prominent in the cell bodies and axons of the mesenchephalic trigeminal nucleus and the pars compacta region of nucleus ambiguus, and in the fibres that comprise the solitary tract, the descending spinal trigeminal tract and the trigeminal and facial nerves. A small proportion of peripherin positive fibres in CN VIII likely arise from cochlear type II spiral ganglion neurons. Peripherin positive fibres were also observed in the inferior cerebellar peduncle and folia in the intermediate zone of the cerebellum. Antibody specificity was confirmed by absence of labelling in hindbrain tissue from peripherin knockout mice. This study shows that in the adult mouse hindbrain, peripherin is expressed in discrete neuronal subpopulations that have sensory, motor and autonomic functions.

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Section: Discussionmentioning

confidence: 94%

Section: Cerebellummentioning

confidence: 98%

Neuronal expression of peripherin, a type III intermediate filament protein, in the mouse hindbrain

Barclay

Noakes

Ryan

et al. 2007

Histochem Cell Biol

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“…Type I and type II axons arborize in parallel to the dorsal and ventral cochlear nuclei in the brainstem; but only type II endings are found within the small cell cap and granule cell layers that envelope the principal nuclei (28)(29)(30)(31)(32). The granule cell domain is thought to be a site for multimodal integration as well as the target of collaterals from olivocochlear efferents (29,30,(33)(34)(35)(36)(37)(38). Whether components of the small cell cap or granule cell layers project to central pain pathways remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

Unmyelinated type II afferent neurons report cochlear damage

Liu

Glowatzki

Fuchs

2015

Proc. Natl. Acad. Sci. U.S.A.

109

102

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In the mammalian cochlea, acoustic information is carried to the brain by the predominant (95%) large-diameter, myelinated type I afferents, each of which is postsynaptic to a single inner hair cell. The remaining thin, unmyelinated type II afferents extend hundreds of microns along the cochlear duct to contact many outer hair cells. Despite this extensive arbor, type II afferents are weakly activated by outer hair cell transmitter release and are insensitive to sound. Intriguingly, type II afferents remain intact in damaged regions of the cochlea. Here, we show that type II afferents are activated when outer hair cells are damaged. This response depends on both ionotropic (P2X) and metabotropic (P2Y) purinergic receptors, binding ATP released from nearby supporting cells in response to hair cell damage. Selective activation of P2Y receptors increased type II afferent excitability by the closure of KCNQ-type potassium channels, a potential mechanism for the painful hypersensitivity (that we term "noxacusis" to distinguish from hyperacusis without pain) that can accompany hearing loss. Exposure to the KCNQ channel activator retigabine suppressed the type II fiber's response to hair cell damage. Type II afferents may be the cochlea's nociceptors, prompting avoidance of further damage to the irreparable inner ear.type II cochlear afferents | ATP | acoustic trauma | hyperacusis | noxacusis T he mammalian cochlea is the most elaborate of vertebrate auditory organs. The elegantly coiled, mechanically tuned cochlear duct and functional differentiation between inner hair cells (IHCs) and outer hair cells (OHCs), afferent and efferent neuronal connections are among the features that enable the widest acoustic frequency range and most complex vocalizations among vertebrate species. This benefit, however, has been gained at a significant cost in the metabolic and mechanical vulnerability of cochlear hair cells and neurons. Loud sound progressively damages type I afferent neurons and OHCs (1). Once damaged beyond repair, these do not regenerate as they do in nonmammalian vertebrates, suggesting that protective mechanisms should exist to preserve cochlear function. Indeed, middle ear reflexes (2) and efferent inhibition of hair cells (3) can mitigate acoustic trauma to some extent. However, a more effective strategy is simply to avoid or withdraw from sources of trauma, by analogy to limb withdrawal triggered by C-fiber activation in skin.Here, we provide evidence that unmyelinated type II cochlear afferents can report cochlear trauma, a potential trigger for nocifensive behavior. Hyperactivity of type II neurons could contribute as well to the paradoxical hypersensitivity to loud sound that can accompany hearing loss, despite diminished type I afferent function. Hyperacusis is a comorbidity in 80% of tinnitus patients (4) suggesting common pathogenic mechanisms (5). In the most severe cases, hyperacusis is described as debilitating "ear pain" (6). The response to trauma by type II afferents may relate most directly to such ...

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“…The highly excitable recepto-neural segment could respond to small synaptic inputs from hair cells and effectively transmit the resulting APs out of the organ of Corti. The presence of Nav channels in the initial segments flanking the type II cell body suggests that these neurons can reliably transmit APs into the cochlear nucleus (Hurd et al, 1999;Benson and Brown, 2004). The speed and rate with which APs arrive in the cochlear nucleus would be slower than for type I ganglion cells, because the rest of the type II pathway consists of very thin, unmyelinated fibers.…”

Section: Nav16 Channels In Type II Ganglion Cellsmentioning

confidence: 99%

Where Is the Spike Generator of the Cochlear Nerve? Voltage-Gated Sodium Channels in the Mouse Cochlea

Hossain¹,

Antic²,

Yang³

et al. 2005

J. Neurosci.

155

143

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The origin of the action potential in the cochlea has been a long-standing puzzle. Because voltage-dependent Na ϩ (Nav) channels are essential for action potential generation, we investigated the detailed distribution of Nav1.6 and Nav1.2 in the cochlear ganglion, cochlear nerve, and organ of Corti, including the type I and type II ganglion cells. In most type I ganglion cells, Nav1.6 was present at the first nodes flanking the myelinated bipolar cell body and at subsequent nodes of Ranvier. In the other ganglion cells, including type II, Nav1.6 clustered in the initial segments of both of the axons that flank the unmyelinated bipolar ganglion cell bodies. In the organ of Corti, Nav1.6 was localized in the short segments of the afferent axons and their sensory endings beneath each inner hair cell. Surprisingly, the outer spiral fibers and their sensory endings were well labeled beneath the outer hair cells over their entire trajectory. In contrast, Nav1.2 in the organ of Corti was localized to the unmyelinated efferent axons and their endings on the inner and outer hair cells. We present a computational model illustrating the potential role of the Nav channel distribution described here. In the deaf mutant quivering mouse, the localization of Nav1.6 was disrupted in the sensory epithelium and ganglion. Together, these results suggest that distinct Nav channels generate and regenerate action potentials at multiple sites along the cochlear ganglion cells and nerve fibers, including the afferent endings, ganglionic initial segments, and nodes of Ranvier.

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Postsynaptic Targets of Type II Auditory Nerve Fibers in the Cochlear Nucleus.

Cited by 40 publications

References 63 publications

Neuronal expression of peripherin, a type III intermediate filament protein, in the mouse hindbrain

Neuronal expression of peripherin, a type III intermediate filament protein, in the mouse hindbrain

Unmyelinated type II afferent neurons report cochlear damage

Where Is the Spike Generator of the Cochlear Nerve? Voltage-Gated Sodium Channels in the Mouse Cochlea

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