Effects of cAMP simulate a late stage of LTP in hippocampal CA1 neurons

Science. 1993 Jun 11;260(5114):1661-4. doi: 10.1126/science.8389057.

Abstract

Hippocampal long-term potentiation (LTP) is thought to serve as an elementary mechanism for the establishment of certain forms of explicit memory in the mammalian brain. As is the case with behavioral memory, LTP in the CA1 region has stages: a short-term early potentiation lasting 1 to 3 hours, which is independent of protein synthesis, precedes a later, longer lasting stage (L-LTP), which requires protein synthesis. Inhibitors of cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA) blocked L-LTP, and analogs of cAMP induced a potentiation that blocked naturally induced L-LTP. The action of the cAMP analog was blocked by inhibitors of protein synthesis. Thus, activation of PKA may be a component of the mechanism that generates L-LTP.

Publication types

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

MeSH terms

  • Action Potentials / drug effects
  • Action Potentials / physiology
  • Animals
  • Cyclic AMP / physiology*
  • Hippocampus / cytology
  • Hippocampus / drug effects
  • Hippocampus / physiology*
  • In Vitro Techniques
  • Male
  • Memory / physiology
  • Neurons / drug effects
  • Neurons / physiology*
  • Protein Kinases / physiology
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, N-Methyl-D-Aspartate / physiology
  • Second Messenger Systems / physiology
  • Time Factors

Substances

  • Receptors, N-Methyl-D-Aspartate
  • Cyclic AMP
  • Protein Kinases