Mechanisms of cAMP-induced sustained activation of extracellular signal-regulated kinase in the hippocampus

Neuroreport. 2014 May 7;25(7):470-4. doi: 10.1097/WNR.0000000000000117.

Abstract

Protein phosphorylation is known to regulate synaptic plasticity and memory. Protein kinases including protein kinase A and extracellular signal-regulated kinase (ERK) play important roles in these processes. Forskolin, a protein kinase A activator, induces long-term potentiation (LTP) in the hippocampus. Forskolin also induces ERK activation, which plays important roles in LTP. However, the mechanisms of forskolin-induced ERK activation are not clearly understood. Here we show that forskolin induces sustained ERK activation in the hippocampal slices. Further, blockade of protein synthesis or transcription inhibits forskolin-induced sustained ERK activation. In contrast, forskolin-induced immediate ERK activation is unaffected by inhibition of protein synthesis or transcription. Sustained ERK activation may contribute to forskolin-induced LTP in the hippocampus.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Colforsin / pharmacology
  • Cyclic AMP / metabolism*
  • Dactinomycin / pharmacology
  • Drug Interactions
  • Emetine / pharmacology
  • Enzyme Activation / drug effects
  • Enzyme Inhibitors / pharmacology
  • Extracellular Signal-Regulated MAP Kinases / metabolism*
  • Hippocampus / drug effects
  • Hippocampus / metabolism*
  • Imidazoles / pharmacology
  • In Vitro Techniques
  • Phosphorylation
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Enzyme Inhibitors
  • Imidazoles
  • 4-(3,4-dibutoxybenzyl)-2-imidazolidinone
  • Dactinomycin
  • Colforsin
  • Cyclic AMP
  • Extracellular Signal-Regulated MAP Kinases
  • Emetine