ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1996
Neurotrophin-3 is a survival factor in vivo for early mouse trigeminal neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 82 citations in OpenAlex.
- Loss of Elp1 disrupts trigeminal ganglion neurodevelopment in a model of familial dysautonomia.eLife · 2022Article
- Corneal neuromediator profiles following laser refractive surgery.Neural regeneration research · 2021Review
- Transcriptional dysregulation in developing trigeminal sensory neurons in the LgDel mouse model of DiGeorge 22q11.2 deletion syndrome.Human molecular genetics · 2020Article
- Development and critical period plasticity of the barrel cortex.The European journal of neuroscience · 2012Review
- Article
- Smooth-muscle-specific expression of neurotrophin-3 in mouse embryonic and neonatal gastrointestinal tract.Cell and tissue research · 2010Article
- Morphometric analysis of embryonic rat trigeminal neurons treated with different neurotrophins.The anatomical record. Part A, Discoveries in molecular, cellular, and evolutionary biology · 2004Article
- Regulation of neuronal survival and death by extracellular signals during development.The EMBO journal · 2003Review
- Neurotrophins: roles in neuronal development and function.Annual review of neuroscience · 2001Review
- Differential effects of NGF and NT-3 on embryonic trigeminal axon growth patterns.The Journal of comparative neurology · 2000Article
- Directional specificity and patterning of sensory axons in trigeminal ganglion-whisker pad cocultures.Brain research. Developmental brain research · 2000Article
- En passant neurotrophic action of an intermediate axonal target in the developing mammalian CNS.Nature · 1999Article
- Perturbation of cell cycle progression and cellular gene expression as a function of herpes simplex virus ICP0.Journal of virology · 1999Article
- Selective regulation of trkC expression by NT3 in the developing peripheral nervous system.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- POU domain factor Brn-3a controls the differentiation and survival of trigeminal neurons by regulating Trk receptor expression.Development (Cambridge, England) · 1999Article
- Expression of Trk receptors in the developing mouse trigeminal ganglion: in vivo evidence for NT-3 activation of TrkA and TrkB in addition to TrkC.Development (Cambridge, England) · 1999Article
- Regulation of neurotrophin-3 expression by epithelial-mesenchymal interactions: the role of Wnt factors.Science (New York, N.Y.) · 1999Article
- Regulation of neurotrophin receptor expression by retinoic acid in mouse sympathetic neuroblasts.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Neurotrophins support the development of diverse sensory axon morphologies.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Evidence for a role of truncated trkC receptor isoforms in mouse development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Mice lacking neurotrophin-3 (NT-3) have been shown previously to be born with severe sensory deficits. This study characterizes the developmental course of this deficit in the trigeminal sensory ganglion, which in NT-3 homozygous mutants contains only 35% of the normal number of neurons at birth. At embryonic day 10.5 (E10.5), normal numbers of neurons, as assessed by expression of neurofilament protein and of total cells, are present in the ganglia of mutant homozygotes. During the next 3 d (E10.5-E13.5), virtually all of the deficit develops, after which mutant animals retain only approximately 30% the normal number of neurons. Quantification of neuronal and neuronal precursor numbers in normal and mutant animals reveals that neurons are specifically depleted in the absence of NT-3. A deficiency in precursor proliferation is only seen after most of the neuronal deficit has developed. Numbers of apoptotic cells in the ganglia of mutant animals are elevated during this same interval, indicating that the neuronal deficit is caused, in large part, by increased cell death of embryonic neurons. To determine sources of NT-3 in the trigeminal system, we examined the expression pattern of beta-galactosidase in mice, in which lacZ has replaced the NT-3 coding exon. E10.5-E11.5 embryos exhibit intense reporter expression throughout the mesenchyme and epithelia of the first branchial arch. Beta-galactosidase expression in E13.5 embryos is largely confined to the oral epithelium and the mesenchyme underlying the skin. Throughout the E10.5-E13.5 interval, the trigeminal ganglion and its targets in the CNS do not express reporter activity. We conclude that NT-3 acts principally as a peripherally derived survival factor for early trigeminal neurons.
Indexed as
Identifiers
8922422PMC2688699W2127020302What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.