ArticleThe Journal of cell biology1995
Regulation of nerve growth factor receptor gene expression in sympathetic neurons during development.
Article in The Journal of cell biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 91 citations in OpenAlex.
- Neurotrophin Responsiveness of Sympathetic Neurons Is Regulated by Rapid Mobilization of the p75 Receptor to the Cell Surface through TrkA Activation of Arf6.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- ProNGF, but Not NGF, Switches from Neurotrophic to Apoptotic Activity in Response to Reductions in TrkA Receptor Levels.International journal of molecular sciences · 2017Article
- Neurotrophins regulate cholinergic synaptic transmission in cultured rat sympathetic neurons through a p75-dependent mechanism.Journal of neurophysiology · 2013Article
- Article
- Neurotrophins and target interactions in the development and regulation of sympathetic neuron electrical and synaptic properties.Autonomic neuroscience : basic & clinical · 2009Review
- p75 and TrkA signaling regulates sympathetic neuronal firing patterns via differential modulation of voltage-gated currents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Abnormal sympathetic nervous system development and physiological dysautonomia in Egr3-deficient mice.Development (Cambridge, England) · 2008Article
- Ankyrin-rich membrane spanning protein plays a critical role in nuclear factor-kappa B signaling.Molecular and cellular neurosciences · 2008Article
- A model for neuronal competition during development.Science (New York, N.Y.) · 2008Article
- Tumor necrosis factor alpha regulates responses to nerve growth factor, promoting neural cell survival but suppressing differentiation of neuroblastoma cells.Molecular biology of the cell · 2008Article
- On the presence of neurotrophin p75 receptor on rat sympathetic cerebrovascular nerves.Journal of molecular histology · 2008Article
- Decreased apoptosome activity with neuronal differentiation sets the threshold for strict IAP regulation of apoptosis.The Journal of cell biology · 2004Article
- The extracellular domain of p75NTR is necessary to inhibit neurotrophin-3 signaling through TrkA.The Journal of biological chemistry · 2001Article
- Neurotrophin-3 promotes the cholinergic differentiation of sympathetic neurons.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- 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
- 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
- Autocrine hepatocyte growth factor provides a local mechanism for promoting axonal growth.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- Bcl-2 accelerates the maturation of early sensory neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- Competitive signaling between TrkA and p75 nerve growth factor receptors determines cell survival.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- Nerve growth factor modulates synaptic transmission between sympathetic neurons and cardiac myocytes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1997Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We used quantitative reverse transcription (RT)/PCR to study the regulation of p75 mRNA and trkA mRNA expression in the developing sympathetic neurons of the mouse superior cervical sympathetic ganglion (SCG) in vivo and in vitro. At E13, the SCG contains proliferating cells that express many features of differentiated neurons. These immature neurons survived in culture without NGF, and NGF did not induce c-fos expression. Low levels of p75 and trkA mRNAs were expressed at this stage in vivo. There was no significant increase in the level of either trkA mRNA or p75 mRNA in E13 control cultures up to 72 h in vitro, and neither NGF nor depolarizing levels of K+ ions (40 mM KC1) affected the expression of trkA mRNA. In E14 cultures, NGF induced c-fos expression in 10-15% of the neurons and enhanced the survival of a similar percentage of neurons. The proportion of neurons responding to NGF increased with age, reaching 90% in E18 cultures. The in vivo level of trkA mRNA increased markedly from E14 onward, but in contrast to sensory neurons (in which p75 and trkA mRNA levels increase in parallel), the level of trkA mRNA initially increased far more rapidly than that of p75 mRNA. After E17, the level of p75 mRNA increased rapidly and approached that of trkA mRNA postnatally, but at no stage did this exceed the level of trkA mRNA. In E14 cultures, the level of trkA mRNA increased in the absence of neurotrophins or 40 mM KC1. The level of p75 mRNA in E14 cultures was enhanced by NGF but was unaffected by 40 mM KC1. Our findings show that NGF receptor expression during the earliest stages of sympathetic neuron development is not affected by depolarization but indicate that by an early developmental stage (between E13 and E14 in vivo), sympathetic neurons become specified to upregulate trkA mRNA in culture independently of added factors. In addition, our findings reveal several distinctive features of p75 mRNA and trkA mRNA expression in sympathetic neurons compared with sensory neurons and provide a plausible explanation for previously observed differences in the effects of a p75 null mutation on the response of sensory and sympathetic neurons during embryonic and postnatal development.
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