Connexin29 Is Highly Expressed in Cochlear Schwann Cells, and It Is Required for the Normal Development and Function of the Auditory Nerve of Mice

Tang, Wenxue; Zhang, Yanping; Chang, Qing; Ahmad, Shoab; Dahlke, Ian; Hong, Yi Ren; Chen, Ping; Paul, David L.; Lin, Xi

doi:10.1523/jneurosci.5055-05.2006

Cited by 72 publications

(65 citation statements)

References 42 publications

(60 reference statements)

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“…MAG is a member of the CNS-derived myelin-based growth inhibitors that also include Nogo and OmgP ( oligodendrocyte myelin glycoprotein). MAG is strongly expressed in the axonal myelin of SG of adult [Martini, 1994] and newborn mice [Tang et al, 2006]. RhoA seems to be a mediator in activation of myelin-based growth inhibitors while p75 NTR -/-can direct RhoA [Yamashita et al, 1999].…”

Section: Discussionmentioning

confidence: 97%

Spiral Ganglion Outgrowth and Hearing Development in p75NTR-Deficient Mice

Brors

Hansen²,

Mlynski³

et al. 2008

Audiol Neurotol

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To explore the role of nerve growth factor receptor p75^NTR during the terminal neuronal development of the mammalian cochlea the onset of hearing and the in vitro response of spiral ganglion neurites to neurotrophin 3 (NT-3), which is known to play a critical role during neonatal inner ear development, were investigated in p75^NTR-deficient mice (p75^NTR–/–). Auditory-evoked brain stem response recordings from p75^NTR–/– and wild-type (WT) littermates were measured from postnatal days (PD) 8 to 23. Additionally, spiral ganglion explants from p75^NTR–/– and WT animals were dissected and cultured in an organotypic tissue culture system. In both groups, spiral ganglion neurite outgrowth was analyzed with and without NT-3 supplementation. No significant differences in the onset of hearing of mutant mice compared to the WT mice were detected, and both groups showed a similar development of hearing until PD 23. After stimulation with NT-3, neurite outgrowth was enhanced in both p75^NTR–/– and WT mice. However, neurites from p75^NTR–/– spiral ganglion explants were longer in both culture conditions. Moreover, NT-3 did not significantly enhance neurite number in p75^NTR–/–, as it did in WT mice. P75^NTR has a remarkable influence on spiral ganglion neurite growth behavior. However, p75^NTR does not seem to be essential for the development of basic hearing function in the first 3 postnatal weeks.

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Section: Discussionmentioning

confidence: 97%

Spiral Ganglion Outgrowth and Hearing Development in p75NTR-Deficient Mice

Brors

Hansen²,

Mlynski³

et al. 2008

Audiol Neurotol

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“…A newly discovered member of the Cx gene family, Cx29, has been found to be expressed in the cochlea [Ahmad et al, 2003;Yang et al, 2005;Tang et al, 2006]. At least 3 heterozygous mutations (c.807A ] T, c.781 + 10C ] G and c.781 + 15C ] T) and 2 heterozygous polymorphisms (781 + 62G ] A and c. * +2 T ] G) of the Cx29 gene have been reported in nonsyndromic deafness patients from Taiwan .…”

Section: Discussionmentioning

confidence: 99%

“…Further studies have also indicated that Cx29 protein is expressed in the mouse or rat cochlea, including in the cochlea neurons, spiral limbus, spiral ligament, organ of Corti, stria vascularis, Schwann cells myelinating the soma and the fiber of spiral ganglion neurons [Yang et al, 2005;Tang et al, 2006]. The Cx29 gene (NM 181538), which contains 2 exons and an open reading frame of 840 base pairs, is localized on chromosome 7q22.1.…”

Section: Introductionmentioning

confidence: 99%

Identification of Novel Variants in the Cx29 Gene of Nonsyndromic Hearing Loss Patients Using Buccal Cells and Restriction Fragment Length Polymorphism Method

Wang¹,

Yang

Lin³

et al. 2009

Audiol Neurotol

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The crucial role of gap junctions, which are composed of connexin (Cx) protein, in auditory functions has been confirmed by numerous studies. Cx29 is a relatively new member of the Cx protein family. In this article, we report variants of the Cx29 gene in 253 unrelated Taiwanese patients with nonsyndromic hearing loss. Thirteen (5.14%) of the 253 patients had variants of Cx29. Five sequence changes (c.43C→G, c.230G→C, c.525T→G, c.781 + 62G→A and c.*2T→G) in the Cx29 gene were detected in the study, of which 3 (c.43C→G, c.230G→C and c.525T→G) were novel variants. One novel compound heterozygote missense variant, c.[43C→G(+) 230G→C], was identified in the Cx29 gene carried by 1 patient, and this variant appears to have been inherited from the mother’s chromosome. In addition, for diagnostic purposes, we developed a restriction fragment length polymorphism method using NaeI and StyI to identify c.43C→G and c.525T→G specific variants of the Cx29 gene, respectively. On the basis of the above results, we suggest that the c.[43C→G(+)230G→C] compound heterozygous variant of Cx29 may be a risk factor for the development of hearing loss in Taiwanese and that the restriction fragment length polymorphism method developed will be clinically useful in identifying variants of the Cx29 gene in patients with hearing loss.

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“…However, Cx29 does not accumulate in gap junctional plaques in vivo in oligodendrocytes or Schwann cells (Altevogt et al 2002;Nagy et al 2003;Altevogt and Paul 2004) or form function gap junctions when expressed in tissue culture cells (Altevogt et al 2002). On the other hand, the Cx29 KO does show a myelin defect but one that is restricted to cell bodies of the spiral ganglion neurons in the organ of Corti (Tang et al 2006). …”

Section: Gap Junctions In Myelin and The Central Nervous Systemmentioning

confidence: 99%

Gap Junctions

Goodenough¹,

Paul²

2009

Cold Spring Harbor Perspectives in Biology

546

440

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Connexin29 Is Highly Expressed in Cochlear Schwann Cells, and It Is Required for the Normal Development and Function of the Auditory Nerve of Mice

Abstract: Connexins (Cxs

Cited by 72 publications

References 42 publications

Spiral Ganglion Outgrowth and Hearing Development in p75<sup>NTR</sup>-Deficient Mice

Spiral Ganglion Outgrowth and Hearing Development in p75<sup>NTR</sup>-Deficient Mice

Identification of Novel Variants in the <i>Cx29</i> Gene of Nonsyndromic Hearing Loss Patients Using Buccal Cells and Restriction Fragment Length Polymorphism Method

Gap Junctions

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