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