Activation of p42/44 mitogen-activated protein kinase pathway in long-term potentiation induced by nicotine in hippocampal CA1 region in rats

Acta Pharmacol Sin. 2001 Aug;22(8):685-90.

Abstract

Aim: To investigate the relationship between activation of p42/44 mitogen-activated protein kinase (MAPK) pathway and hippocampal long term potentiation (LTP) induced by nicotine in area CA 1.

Methods: Extracellular recording of population spike (PS) was performed within the pyramidal cell layer of hippocampal area CA1 in vitro; Western blot analysis was employed to detect the active phosphorylated state and the total protein expression of p42/44 MAPK.

Results: PD98059 concentration-dependently (25 micromol/L, 50 micromol/L) attenuated the induction of LTP induced by nicotine 10 micromol/L; both p42 and p44 MAPK were activated with their total protein expression increasing in CA1 subregion in response to LTP induced by nicotine.

Conclusion: Activation of p42/44 MAPK pathway is required for hippocampal LTP induced by nicotine.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Flavonoids / pharmacology
  • Hippocampus / physiology*
  • Long-Term Potentiation / drug effects*
  • Mitogen-Activated Protein Kinase 1 / metabolism*
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases / metabolism*
  • Nicotine / pharmacology*
  • Phosphorylation
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction

Substances

  • Flavonoids
  • Nicotine
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases
  • 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one