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Title: Uncoupling nicotine mediated motoneuron axonal pathfinding errors and muscle degeneration in zebrafish

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 amore » direct effect of nicotine exposure on nervous system development.« less

Authors:
 [1];  [2]
  1. Department of Biological Sciences, Louisiana State University, Baton Rouge, Louisiana, 70803 (United States)
  2. Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis Oregon, 97331 (United States)
Publication Date:
OSTI Identifier:
21272552
Resource Type:
Journal Article
Journal Name:
Toxicology and Applied Pharmacology
Additional Journal Information:
Journal Volume: 237; Journal Issue: 1; Other Information: DOI: 10.1016/j.taap.2008.06.025; PII: S0041-008X(08)00306-2; Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0041-008X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; EMBRYOS; MUSCLES; MUTANTS; NERVE CELLS; NERVOUS SYSTEM; NICOTINE; POTATOES; RECEPTORS; VERTEBRATES

Citation Formats

Welsh, Lillian, Tanguay, Robert L, and Svoboda, Kurt R. Uncoupling nicotine mediated motoneuron axonal pathfinding errors and muscle degeneration in zebrafish. United States: N. p., 2009. Web. doi:10.1016/j.taap.2008.06.025.
Welsh, Lillian, Tanguay, Robert L, & Svoboda, Kurt R. Uncoupling nicotine mediated motoneuron axonal pathfinding errors and muscle degeneration in zebrafish. United States. https://doi.org/10.1016/j.taap.2008.06.025
Welsh, Lillian, Tanguay, Robert L, and Svoboda, Kurt R. 2009. "Uncoupling nicotine mediated motoneuron axonal pathfinding errors and muscle degeneration in zebrafish". United States. https://doi.org/10.1016/j.taap.2008.06.025.
@article{osti_21272552,
title = {Uncoupling nicotine mediated motoneuron axonal pathfinding errors and muscle degeneration in zebrafish},
author = {Welsh, Lillian and Tanguay, Robert L and Svoboda, Kurt R.},
abstractNote = {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.},
doi = {10.1016/j.taap.2008.06.025},
url = {https://www.osti.gov/biblio/21272552}, journal = {Toxicology and Applied Pharmacology},
issn = {0041-008X},
number = 1,
volume = 237,
place = {United States},
year = {Fri May 15 00:00:00 EDT 2009},
month = {Fri May 15 00:00:00 EDT 2009}
}