Distinct roles for Sema3A, Sema3F, and an unidentified trophic factor in controlling the advance of geniculate axons to gustatory lingual epithelium

Vilbig, Ryan; Cosmano, Jason; Giger, Roman J.; Rochlin, M. William

doi:10.1007/s11068-005-3329-8

Cited by 24 publications

(39 citation statements)

References 51 publications

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“…As discussed next, our current results support a straightforward interpretation of the in vivo neurotrophin perturbation studies. Substantial parallels between in vivo and in vitro observations were also found in our previous studies of other diffusible cues [58][59][60] . Our in vitro findings combined with localization data would have predicted the results from in vivo studies.…”

Section: Discussionsupporting

confidence: 84%

Brain-Derived Neurotrophic Factor Attracts Geniculate Ganglion Neurites during Embryonic Targeting

Hoshino

Vatterott²,

Egwiekhor³

et al. 2010

Dev Neurosci

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Geniculate axons are initially guided to discrete epithelial placodes in the lingual and palatal epithelium that subsequently differentiate into taste buds. In vivo approaches show that brain-derived neurotrophic factor (BDNF) mRNA is concentrated in these placodes, that BDNF is necessary for targeting taste afferents to these placodes, and that BDNF misexpression disrupts guidance. We used an in vitro approach to determine whether BDNF may act directly on geniculate axons as a trophic factor and as an attractant, and whether there is a critical period for responsiveness to BDNF. We show that BDNF promotes neurite outgrowth from geniculate ganglion explants dissected from embryonic day (E) 15, E18, infant, and adult rats cultured in collagen gels, and that there is a concentration optimum for neurite extension. Gradients of BDNF derived from slow-release beads caused the greatest bias in neurite outgrowth at E15, when axons approach the immature gustatory papillae. Further, neurites advanced faster toward the BDNF bead than away from it, even if the average amount of neurotrophic factor encountered was the same. We also found that neurites that contact BDNF beads did not advance beyond them. At E18, when axons would be penetrating pregustatory epithelium in vivo, BDNF continued to exert a tropic effect on geniculate neurites. However, at postnatal and adult stages, the influence of BDNF was predominantly trophic. Our data support a role for BDNF acting as an attractant for geniculate axons during a critical period that encompasses initial targeting but not at later stages.

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Section: Discussionsupporting

confidence: 84%

Brain-Derived Neurotrophic Factor Attracts Geniculate Ganglion Neurites during Embryonic Targeting

Hoshino

Vatterott²,

Egwiekhor³

et al. 2010

Dev Neurosci

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“…For instance, NT4/5, but not BDNF, enhances the responses of geniculate neurons to Sema3A and Sema3F [78]. In mice that over express NT4/5 in the epithelium, chorda tympani fibers remain below the surface as if repelled by the lingual epithelium [80].…”

Section: Development Of the Geniculate And Petrosal Gangliamentioning

confidence: 99%

Factors that regulate embryonic gustatory development

Krimm

2007

BMC Neurosci

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Numerous molecular factors orchestrate the development of the peripheral taste system. The unique anatomy/function of the taste system makes this system ideal for understanding the mechanisms by which these factors function; yet the taste system is underutilized for this role. This review focuses on some of the many factors that are known to regulate gustatory development, and discusses a few topics where more work is needed. Some attention is given to factors that regulate epibranchial placode formation, since gustatory neurons are thought to be primarily derived from this region. Epibranchial placodes appear to arise from a pan-placodal region and a number of regulatory factors control the differentiation of individual placodes. Gustatory neuron differentiation is regulated by a series of transcription factors and perhaps bone morphongenic proteins (BMP). As neurons differentiate, they also proliferate such that their numbers exceed those in the adult, and this is followed by developmental death. Some of these cell-cycling events are regulated by neurotrophins. After gustatory neurons become post-mitotic, axon outgrowth occurs. Axons are guided by multiple chemoattractive and chemorepulsive factors, including semaphorins, to the tongue epithelium. Brain derived neurotrophic factor (BDNF), functions as a targeting factor in the final stages of axon guidance and is required for gustatory axons to find and innervate taste epithelium. Numerous factors are involved in the development of gustatory papillae including Sox-2, Sonic hedge hog and Wnt-β-catenin signaling. It is likely that just as many factors regulate taste bud differentiation; however, these factors have not yet been identified. Studies examining the molecular factors that regulate terminal field formation in the nucleus of the solitary tract are also lacking. However, it is possible that some of the factors that regulate geniculate ganglion development, outgrowth, guidance and targeting of peripheral axons may have the same functions in the gustatory CNS.

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“…However, in the taste system, although any of these guidance molecules may regulate axon guidance of geniculate neurons, most of them remain un-investigated except semaphorin 3A (Sema3A). Sema3A is expressed in the tongue and required for both trigeminal and geniculate axon guidance ( [62], [54], [63] [68], [69], [70]). …”

Section: The Development Of Geniculate Ganglionmentioning

confidence: 99%

“…Sema3A repels geniculate ganglion axons in vitro, and Sema3A mutant mice showed increased taste innervation to the middle line of the tongue [54]. In addition, these repellent effects of Sema3A were neurotrophin dependent, both BDNF and NT-4 stimulated taste nerve outgrowth were repelled by Sema3A during development ( [63]). Furthermore, DRG neurons in p75 -/-mice are hypersensitive to the Sema3A, indicating that p75 is an important modulator of Sema3A activity ( [152]).…”

Section: Taste Buds Are Lost and Taste Bud Innervation Is Reduced At mentioning

confidence: 99%

“…Furthermore, DRG neurons in p75 -/-mice are hypersensitive to the Sema3A, indicating that p75 is an important modulator of Sema3A activity ( [152]). Lastly, Sema3F, which is also expressing in the tongue, may also be involved in loss of taste innervation in the p75 -/-mice due to its repellent effect of NT-4 dependent neurite outgrowth ( [63], [55]). …”

Section: Taste Buds Are Lost and Taste Bud Innervation Is Reduced At mentioning

Distinct roles for Sema3A, Sema3F, and an unidentified trophic factor in controlling the advance of geniculate axons to gustatory lingual epithelium

Cited by 24 publications

References 51 publications

Brain-Derived Neurotrophic Factor Attracts Geniculate Ganglion Neurites during Embryonic Targeting

Brain-Derived Neurotrophic Factor Attracts Geniculate Ganglion Neurites during Embryonic Targeting

Factors that regulate embryonic gustatory development

The role of neurotrophin receptors in taste development.

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