Nicotinic receptors mediate changes in spinal motoneuron development and axonal pathfinding in embryonic zebrafish exposed to nicotine

J Neurosci. 2002 Dec 15;22(24):10731-41. doi: 10.1523/JNEUROSCI.22-24-10731.2002.

Abstract

We show that transient exposure of embryonic zebrafish to nicotine delays the development of secondary spinal motoneurons. Furthermore, there is a long-lasting alteration in axonal pathfinding in secondary motoneurons that is not ameliorated by drug withdrawal. These effects of nicotine were reversed by mammalian nicotinic receptor antagonists. Coupled with these changes is a long-term alteration in swimming behavior. Our results show that transient embryonic exposure to nicotine leads to long-lasting effects on the vertebrate nervous system. These results also demonstrate that the zebrafish is a useful model to examine the effects of nicotine specifically, and drugs of abuse in general, on the development of the CNS in vertebrates.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Axons / drug effects
  • Axons / ultrastructure*
  • Behavior, Animal / drug effects
  • Biomarkers / analysis
  • Cell Differentiation
  • Cell Line
  • Embryo, Nonmammalian / anatomy & histology
  • Embryo, Nonmammalian / chemistry
  • Embryo, Nonmammalian / drug effects
  • Green Fluorescent Proteins
  • Kinetics
  • Luminescent Proteins / genetics
  • Luminescent Proteins / metabolism
  • Motor Neurons / cytology*
  • Motor Neurons / drug effects
  • Nervous System / drug effects
  • Nervous System / growth & development
  • Nicotine / pharmacology*
  • Receptors, Nicotinic / physiology*
  • Spinal Cord / cytology
  • Spinal Cord / embryology*
  • Swimming
  • Transgenes
  • Zebrafish / anatomy & histology
  • Zebrafish / embryology
  • Zebrafish / physiology

Substances

  • Biomarkers
  • Luminescent Proteins
  • Receptors, Nicotinic
  • Green Fluorescent Proteins
  • Nicotine