Expression patterns of neurotrophin and their receptor mRNAs in the rat inner ear

Ylikoski, Jukka; Pirvola, Ulla; Moshnyakov, Maxim; Palgi, Jaan; Arumäe, Urmas; Saarma, Märt

doi:10.1016/0378-5955(93)90202-c

Cited by 284 publications

(290 citation statements)

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“…In the hippocampus, TrkB and TrkC signaling cooperate to promote the survival of the DG granular neurons (Minichiello and Klein, 1996). The signaling of TrkB and its major ligand, BDNF (brain-derived neurotrophic factor), is particularly important for the development of vestibular ganglion neurons, while signaling through TrkC and its high affinity ligand NT-3 (neurotrophin-3) is primarily required for the survival and innervations of the acoustic ganglia (Wheeler et al, 1994;Ylikoski et al, 1993). Similar to the results of the present study, the vestibular ganglion cells of BDNF/Bax double null mice did not undergo cell death but rather exhibited severe defects in the innervation of the canal cristae (Hellard et al, 2004), suggesting that the ND -/-Bax -/-vestibular neurons may suffer from innervation defects.…”

Section: Discussionmentioning

confidence: 99%

NeuroD Regulates Neuronal Migration

Kim

2013

Molecules and Cells

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NeuroD is required for the survival of many subtypes of developing neurons in the vertebrate central nervous system. Because NeuroD-deficient neurons in the hippocampus, cerebellum, and inner ear die prematurely in the early stage of neurogenesis, the role of NeuroD during the later stages of neurogenesis of these cell subtypes is not well understood. In addition, the mechanism of NeuroDdeficient neuronal death has not been investigated. It was hypothesized that NeuroD-dependent neuronal death occurs through a Bax-dependent apoptotic pathway. Based on this hypothesis, this study attempted to rescue neuronal cell death by deleting the Bax gene in NeuroD null mice to investigate the role of NeuroD in surviving neurons. The NeuroD and Bax double null mice displayed a decrease in the number of apoptotic cells in the hippocampus and the cerebellum and the rescue of vestibulocochlear ganglion (VCG) neurons that failed to migrate and innervate. In addition, at E13.5, the NeuroD -/-Bax -/-VCG neurons failed to express TrkB and TrkC, which are known to be essential for the survival of those neurons. These data suggest that neuronal death in NeuroD null mice is mediated by Bax-dependent apoptosis and that NeuroD is required for the migration of VCG neurons. Finally, these data show that TrkB and TrkC expression in E13.5 VCG neurons requires NeuroD and that TrkB and TrkC expression may be necessary for the normal migration and innervations of those neurons.

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Section: Discussionmentioning

confidence: 99%

NeuroD Regulates Neuronal Migration

Kim

2013

Molecules and Cells

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“…At P5, NT-3 expression is low in auditory hair cells, and BDNF is not expressed (Pirvola et al, 1994;Wheeler et al, 1994), concomitant with a postnatal reorganization of afferent SGN synapses and period of SGN death during which ϳ20% of SGNs are lost (Rueda et al, 1987). In mature organ of Corti, NT-3 is expressed in the inner hair cells, and BDNF is not expressed (Ylikoski et al, 1993;Pirvola et al, 1994;Schecterson and Bothwell, 1994;Wheeler et al, 1994). Thus, if a hair cell-derived neurotrophin is necessary for support of mature type I SGNs, it is NT-3.…”

Section: Support By Neurotrophinsmentioning

confidence: 99%

“…However, the SGNs, which express both TrkB and TrkC (Ylikoski et al, 1993;Pirvola et al, 1994;Schecterson and Bothwell, 1994), require only NT-3 for survival. Mice homozygous for NT-3 knockout are born lacking Ͼ85% of the SGNs (Fariñas et al, 1994;Ernfors et al, 1995), whereas mice homozygous for BDNF knockout show only a small loss of SGNs at birth (Conover et al, 1995;Ernfors et al, 1995).…”

Section: Support By Neurotrophinsmentioning

confidence: 99%

“…SGNs can receive target-derived neurotrophic support by either BDNF or NT-3 in vivo, because both are expressed in the cochlear nucleus (Lefebvre et al, 1994). Type I SGNs can receive presynaptic neurotrophic support from NT-3, expressed in inner hair cells (Ylikoski et al, 1993;Schecterson and Bothwell, 1994).…”

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confidence: 99%

“…SGNs express TrkB and TrkC (Ylikoski et al, 1993;Schecterson and Bothwell, 1994) and are supported by BDNF, NT-4, and NT-3 in vitro (Avila et al, 1993;Vazquez et al, 1994;Zheng et al, 1995). SGNs can receive target-derived neurotrophic support by either BDNF or NT-3 in vivo, because both are expressed in the cochlear nucleus (Lefebvre et al, 1994).…”

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confidence: 99%

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Trophic Support of Cultured Spiral Ganglion Neurons by Depolarization Exceeds and Is Additive with that by Neurotrophins or cAMP and Requires Elevation of [Ca²⁺]_iwithin a Set Range

Kay²,

1997

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Differential expression of brain-derived neurotrophic factor and neurotrophin 3 mRNA in lingual papillae and taste buds indicates roles in gustatory and somatosensory innervation

1996

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Although many studies have demonstrated the dependency of taste bud function and/or survival on intact innervation, relatively few have dealt with the development of taste bud innervation. Using in situ hybridization histochemistry, we show that brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT3) mRNA are expressed in a specific pattern in the taste buds, tongue papillae, and lingual epithelium during development and that expression persists into adulthood. BDNF mRNA is expressed in a fraction of the taste cells of the developing and adult taste buds in rats, showing different labeling intensities among the labeled cells. NT3 and mRNA seems to be located in areas other than those where BDNF mRNA is expressed, mainly in the superior epithelial surfaces of circumvallate papillae, the outer surface epithelium of foliate papilae, the superior surface and the lateral epithelium of the fungiform papillae, and the epithelium of the filiform papillae. NT3 mRNA labeling is also observed among muscle and connective tissue of the tongue. The morphological appearance, expression of NT3 mRNA, and ramification of nerve fibers in defined epithelial structures in the posterior wall of the anterior filiform papillae suggest the existence of a mechanosensory apparatus in these papillae. Nerve growth factor and neurotrophin 4 probes did not give rise to selective labeling in tongue, although their presence cannot be totally excluded. Based on present and prior studies, we suggest that BDNF is needed during initiation and for maintenance of gustatory innervation of taste buds and gustatory papillae and that NT3 is mainly needed for somatosensory innervation of the tongue.

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Expression patterns of neurotrophin and their receptor mRNAs in the rat inner ear

Cited by 284 publications

References 52 publications

NeuroD Regulates Neuronal Migration

NeuroD Regulates Neuronal Migration

Trophic Support of Cultured Spiral Ganglion Neurons by Depolarization Exceeds and Is Additive with that by Neurotrophins or cAMP and Requires Elevation of [Ca²⁺]_iwithin a Set Range

Differential expression of brain-derived neurotrophic factor and neurotrophin 3 mRNA in lingual papillae and taste buds indicates roles in gustatory and somatosensory innervation

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Expression patterns of neurotrophin and their receptor mRNAs in the rat inner ear

Cited by 284 publications

References 52 publications

NeuroD Regulates Neuronal Migration

NeuroD Regulates Neuronal Migration

Trophic Support of Cultured Spiral Ganglion Neurons by Depolarization Exceeds and Is Additive with that by Neurotrophins or cAMP and Requires Elevation of [Ca2+]iwithin a Set Range

Differential expression of brain-derived neurotrophic factor and neurotrophin 3 mRNA in lingual papillae and taste buds indicates roles in gustatory and somatosensory innervation

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Trophic Support of Cultured Spiral Ganglion Neurons by Depolarization Exceeds and Is Additive with that by Neurotrophins or cAMP and Requires Elevation of [Ca²⁺]_iwithin a Set Range