ArticleToxicology and applied pharmacology2009
Uncoupling nicotine mediated motoneuron axonal pathfinding errors and muscle degeneration in zebrafish.
Article in Toxicology and applied pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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.
The trial behind it
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
12 citing papers in PubMed, 34 citations in OpenAlex.
- Modeling neuromuscular diseases in zebrafish.Frontiers in molecular neuroscience · 2022Review
- Opportunities and challenges for using the zebrafish to study neuronal connectivity as an endpoint of developmental neurotoxicity.Neurotoxicology · 2018Review
- Impact of Nicotine Exposure on Hair Cell Toxicity and Embryotoxicity During Zebrafish Development.Clinical and experimental otorhinolaryngology · 2018Article
- Zebrafish: A Model for the Study of Toxicants Affecting Muscle Development and Function.International journal of molecular sciences · 2016Review
- Article
- Motoneuron axon pathfinding errors in zebrafish: differential effects related to concentration and timing of nicotine exposure.Toxicology and applied pharmacology · 2015Article
- Zebrafish as a model system for environmental health studies in the grade 9-12 classroom.Zebrafish · 2014Article
- Activation of α2A-containing nicotinic acetylcholine receptors mediates nicotine-induced motor output in embryonic zebrafish.The European journal of neuroscience · 2014Article
- Zebrafish: a model for the study of addiction genetics.Human genetics · 2012Review
- Zebrafish for the study of the biological effects of nicotine.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2011Review
- Secondary motoneurons in juvenile and adult zebrafish: axonal pathfinding errors caused by embryonic nicotine exposure.The Journal of comparative neurology · 2009Article
- Embryonic motor activity and implications for regulating motoneuron axonal pathfinding in zebrafish.The European journal of neuroscience · 2008Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Zebrafish embryos offer a unique opportunity to investigate the mechanisms by which nicotine exposure impacts early vertebrate development. Embryos exposed to nicotine become functionally paralyzed by 42 hpf suggesting that the neuromuscular system is compromised in exposed embryos. We previously demonstrated that secondary spinal motoneurons in nicotine-exposed embryos were delayed in development and that their axons made pathfinding errors (Svoboda, K.R., Vijayaraghaven, S., Tanguay, R.L., 2002. Nicotinic receptors mediate changes in spinal motoneuron development and axonal pathfinding in embryonic zebrafish exposed to nicotine. J. Neurosci. 22, 10731-10741). In that study, we did not consider the potential role that altered skeletal muscle development caused by nicotine exposure could play in contributing to the errors in spinal motoneuron axon pathfinding. In this study, we show that an alteration in skeletal muscle development occurs in tandem with alterations in spinal motoneuron development upon exposure to nicotine. The alteration in the muscle involves the binding of nicotine to the muscle-specific AChRs. The nicotine-induced alteration in muscle development does not occur in the zebrafish mutant (sofa potato, [sop]), which lacks muscle-specific AChRs. Even though muscle development is unaffected by nicotine exposure in sop mutants, motoneuron axonal pathfinding errors still occur in these mutants, indicating a direct effect of nicotine exposure on nervous system development.
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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.