Activation of orexin neurons by acute nicotine

Eur J Pharmacol. 2006 Mar 27;535(1-3):172-6. doi: 10.1016/j.ejphar.2006.02.021. Epub 2006 Mar 6.

Abstract

The hypothalamus is a prominent central site of action of nicotine but the phenotype of nicotine-sensitive neurons in this region has not been fully described. Hypothalamic orexin neurons are important regulators of state-dependent behavior, arousal and feeding. Here, we treated rats with acute nicotine and quantitated Fos expression as a marker of neuronal activation. Nicotine increased the percentage of orexin neurons expressing Fos without a significant effect on non-orexin neurons. This effect was attenuated by the nicotinic antagonists mecamylamine and dihydro-beta-erythroidine, implicating alpha4beta2-containing nicotinic receptors. The orexin system is likely to play an important role in the coordination of physiological and behavioral responses to acute nicotine treatment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Dihydro-beta-Erythroidine / pharmacology
  • Ganglionic Stimulants / pharmacology
  • Hypothalamus / cytology
  • Hypothalamus / drug effects
  • Hypothalamus / metabolism
  • Immunohistochemistry
  • Intracellular Signaling Peptides and Proteins / metabolism*
  • Male
  • Mecamylamine / pharmacology
  • Neurons / drug effects*
  • Neurons / metabolism
  • Neuropeptides / metabolism*
  • Nicotine / pharmacology*
  • Nicotinic Antagonists / pharmacology
  • Orexins
  • Proto-Oncogene Proteins c-fos / metabolism
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Ganglionic Stimulants
  • Intracellular Signaling Peptides and Proteins
  • Neuropeptides
  • Nicotinic Antagonists
  • Orexins
  • Proto-Oncogene Proteins c-fos
  • Dihydro-beta-Erythroidine
  • Mecamylamine
  • Nicotine