ArticleThe Journal of cell biology1994
Ca2+ influx and neurite growth in response to purified N-cadherin and laminin.
Article in The Journal of cell biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.
- Cell adhesion and intracellular calcium signaling in neurons.Cell communication and signaling : CCS · 2013Pooled it
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- Revisiting Netrin-1: One Who Guides (Axons).Frontiers in cellular neuroscience · 2018Review
- Opposing Effects of Neuronal Activity on Structural Plasticity.Frontiers in neuroanatomy · 2016Review
- CDH2 and CDH11 act as regulators of stem cell fate decisions.Stem cell research · 2015Review
- Article
- The potential roles of a laminin receptor in adhesion and apoptosis of cells of the marine bivalve Meretrix meretrix.PloS one · 2012Article
- Calcium channel blockade in embryonic cardiac progenitor cells disrupts normal cardiac cell differentiation.Stem cells and development · 2010Article
- N-cadherin is an in vivo substrate for protein tyrosine phosphatase sigma (PTPsigma) and participates in PTPsigma-mediated inhibition of axon growth.Molecular and cellular biology · 2007Article
- N-cadherin signaling in synapse formation and neuronal physiology.Molecular neurobiology · 2006Review
- The tissue plasminogen activator-plasmin system participates in the rewarding effect of morphine by regulating dopamine release.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Intracellular signaling by the neural cell adhesion molecule.Neurochemical research · 2003Review
- Rapid neuromodulatory actions of integrin ligands.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- Stimulus history alters behavioral responses of neuronal growth cones.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- A role for voltage-gated potassium channels in the outgrowth of retinal axons in the developing visual system.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Local presentation of substrate molecules directs axon specification by cultured hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Nuclear and cytoplasmic free calcium level changes induced by elastin peptides in human endothelial cells.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Laminin directs growth cone navigation via two temporally and functionally distinct calcium signals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The signaling mechanisms underlying neurite growth induced by cadherins and integrins are incompletely understood. In our experiments, we have examined these mechanisms using purified N-cadherin and laminin (LN). We find that unlike the neurite growth induced by fibroblastic cells expressing transfected N-cadherin (Doherty, P., and F.S. Walsh. 1992. Curr. Opin. Neurobiol. 2:595-601), growth induced by purified N-cadherin in chick ciliary ganglion (CG), sensory, or forebrain neurons is not sensitive to inhibition by pertussis toxin. Using fura-2 imaging of single cells, we show that soluble N-cadherin induces Ca2+ increases in CG neuron cell bodies, and, importantly, in growth cones. In contrast, N-cadherin can induce Ca2+ decreases in glial cells. N-cadherin-induced neuronal Ca2+ responses are sensitive to Ni2+, but are relatively insensitive to diltiazem and omega-conotoxin. Similarly, neurite growth induced by purified N-cadherin is inhibited by Ni2+, but is unaffected by diltiazem and conotoxin. Soluble LN also induced small Ca2+ responses in CG neurons. LN-induced neurite growth, like that induced by N-cadherin, is insensitive to diltiazem and conotoxin, but is highly sensitive to Ni2+ inhibition. K+ depolarization experiments suggest that voltage-dependent Ca2+ influx pathways in CG neurons (cell bodies and growth cones) are largely blocked by the combination of diltiazem and Ni2+. Our results demonstrate that cadherin signaling involves cell type-specific Ca2+ changes in responding cells, and in particular, that N-cadherin can cause Ca2+ increases in neuronal growth cones. Our findings are consistent with the current idea that distinct neuronal transduction pathways exist for cell adhesion molecules compared with integrins, but suggest that the involvement of Ca2+ signals in both of these pathways is more complex than previously appreciated.
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