Reciprocal signaling between spiral ganglion neurons and Schwann cells involves neuregulin and neurotrophins

Hansen, Marlan R.; Vijapurkar, Ulka; Koland, John G.; Green, Steven H.

doi:10.1016/s0378-5955(01)00360-4

Cited by 105 publications

(116 citation statements)

References 94 publications

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“…Morley (1998), using in situ hybridization, reported that SGNs are the only cochlear cells that express NRG1. Hansen et al (2001) found NRG1 immunoreactivity in the SGNs and in their peripheral axons, suggesting that NRG1 produced by the SGNs is transported to the organ of Corti, where it could be released. Our immunostaining with NRG1 is in agreement with these observations ( Fig.…”

Section: Discussionmentioning

confidence: 89%

“…In the developing sympathetic nervous system, NRG1 produced by neuroblasts was shown to promote NT3 production by neighboring non-neuronal cells, which in turn promotes neuroblast survival and further differentiation (Verdi et al, 1996). Hansen et al (2001) showed that NRG1 negatively regulates NT3 expression in spiral ganglion Schwann cells in culture at the same time that it induces their proliferation, suggesting that NRG1 and NT3 mediate reciprocal interactions between SGNs and Schwann cells. These observations, in conjunction with our results, suggest that SGNs may use NRG1 to regulate NT3 expression differently in different cell populations in the cochlea.…”

Section: Discussionmentioning

confidence: 99%

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Survival of Adult Spiral Ganglion Neurons Requires erbB Receptor Signaling in the Inner Ear

Stanković¹,

Río²,

Xia³

et al. 2004

J. Neurosci.

183

187

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Degeneration of cochlear sensory neurons is an important cause of hearing loss, but the mechanisms that maintain the survival of adult cochlear sensory neurons are not clearly defined. We now provide evidence implicating the neuregulin (NRG)-erbB receptor signaling pathway in this process. We found that NRG1 is expressed by spiral ganglion neurons (SGNs), whereas erbB2 and erbB3 are expressed by supporting cells of the organ of Corti, suggesting that these molecules mediate interactions between these cells. Transgenic mice in which erbB signaling in adult supporting cells is disrupted by expression of a dominant-negative erbB receptor show severe hearing loss and 80% postnatal loss of type-I SGNs without concomitant loss of the sensory cells that they contact. Quantitative RT-PCR analysis of neurotrophic factor expression shows a specific downregulation in expression of neurotrophin-3 (NT3) in the transgenic cochleas before the onset of neuronal death. Because NT3 is critical for survival of type I SGNs during development, these results suggest that it plays similar roles in the adult. Together, the data indicate that adult cochlear supporting cells provide critical trophic support to the neurons, that survival of postnatal cochlear sensory neurons depends on reciprocal interactions between neurons and supporting cells, and that these interactions are mediated by NRG and neurotrophins.

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Survival of Adult Spiral Ganglion Neurons Requires erbB Receptor Signaling in the Inner Ear

Stanković¹,

Río²,

Xia³

et al. 2004

J. Neurosci.

183

187

View full text Add to dashboard Cite

show abstract

“…11). Figure 11A-C shows that most of Sox2 + cells stain positively for S100, a commonly used Schwann cell marker for mouse and rat auditory nerve (Hansen et al 2001;Hurley et al 2007;Whitlon et al 2009). Dual immunostaining of Sox2 and Sox10 showed that the majority of Sox2 + cells were co-labeled with Sox10 in ouabain-treated nerves (Fig.…”

Section: Sox2 + Expression In Normal and Injured Auditory Nervementioning

confidence: 99%

“…In fact, these glial cells form myelin, maintain homeostasis, and may play a role in many pathological conditions (Romand et al 1980;Romand and Romand 1990;Hansen et al 2001;Morris et al 2006;Hurley et al 2007;Whitlon et al 2009;Wang et al 2010). A previous in vitro study suggests that Schwann cells provide neurotrophic support to the auditory nerve through a reciprocal signaling mechanism (Hansen et al 2001). In the absence of ErbB2, an essential protein for the development of Schwann cells, there is an associated abnormal innervation of the organ of Corti during inner ear development (Morris et al 2006).…”

Section: Introductionmentioning

confidence: 99%

Sox2 Up-regulation and Glial Cell Proliferation Following Degeneration of Spiral Ganglion Neurons in the Adult Mouse Inner Ear

Lang

Kilpatrick

et al. 2010

JARO

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In the present study, glial cell responses to spiral ganglion neuron (SGN) degeneration were evaluated using a murine model of auditory neuropathy. Ouabain, a well-known Na,K-ATPase inhibitor, has been shown to induce SGN degeneration while sparing hair cell function. In addition to selectively removing type I SGNs, ouabain leads to hyperplasia and hypertrophy of glia-like cells in the injured auditory nerves. As the transcription factor Sox2 is predominantly expressed in proliferating and undifferentiated neural precursors during neurogenesis, we sought to examine Sox2 expression patterns following SGN injury by ouabain. Real-time RT-PCR and Western blot analyses of cochlea indicated a significant increase in Sox2 expression by 3 days posttreatment with ouabain. Cells incorporating bromodeoxyuridine (BrdU) and expressing Sox2 were counted in the auditory nerves of control and ouabain-treated ears. The glial phenotype of Sox2 + cells was identified by two neural glial markers: S100 and Sox10. The number of Sox2 + glial cells significantly increased at 3 days post-treatment and reached its maximum level at 7 days post-treatment. Similarly, the number of BrdU + cells increased at 3 and 7 days post-treatment in the injured nerves. Quantitative analysis with dual-immunostaining procedures indicated that about 70% of BrdU + cells in the injured nerves were Sox2 + glial cells. These results demonstrate that up-regulation of Sox2 expression is associated with increased cell proliferation in the auditory nerve after injury.

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“…Exactly what regulates changes in neurotrophic factor expression in Schwann cells is not known. There is evidence, however, that neuronal NRG can regulate glial neurotrophic factor expression (Verdi et al, 1996;Hansen et al, 2001), raising the possibility of a reciprocal feedback loop between axonal NRG and Schwann cell neurotrophic factors.…”

Section: Rapid Axoglial Communication Through Schwann Cell Neurotrophmentioning

confidence: 99%

Rapid Axoglial Signaling Mediated by Neuregulin and Neurotrophic Factors

Esper¹,

Loeb²

2004

J. Neurosci.

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During peripheral nervous system development, Schwann cells are precisely matched to the axons that they support. This is mediated by axonal neuregulins that are essential for Schwann cell survival and differentiation. Here, we show that sensory and motor axons rapidly release heparin-binding forms of neuregulin in response to Schwann cell-derived neurotrophic factors in a dose-dependent manner. Neuregulin release occurs within minutes, is saturable, and occurs from axons that were isolated using a newly designed chamber slide apparatus. Although NGF and glial cell line-derived neurotrophic factor (GDNF) were the most potent neurotrophic factors to release neuregulin from sensory neurons, GDNF and BDNF were most potent for motor neurons and were the predominant neuregulin-releasing neurotrophic factors produced by cultured Schwann cells. Comparable levels of neuregulin could be released at a similar rate from neurons after protein kinase C activation with the phorbol ester, phorbol 12-myristate 13-acetate, which has also been shown to promote the cleavage and release of neuregulin from its transmembrane precursor. The rapid release of neuregulin from axons in response to Schwann cell-derived neurotrophic factors may be part of a spatially restricted system of communication at the axoglial interface important for proper peripheral nerve development, function, and repair.

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Reciprocal signaling between spiral ganglion neurons and Schwann cells involves neuregulin and neurotrophins

Cited by 105 publications

References 94 publications

Survival of Adult Spiral Ganglion Neurons Requires erbB Receptor Signaling in the Inner Ear

Survival of Adult Spiral Ganglion Neurons Requires erbB Receptor Signaling in the Inner Ear

Sox2 Up-regulation and Glial Cell Proliferation Following Degeneration of Spiral Ganglion Neurons in the Adult Mouse Inner Ear

Rapid Axoglial Signaling Mediated by Neuregulin and Neurotrophic Factors

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