Protein kinase A inhibitors prevent the maintenance of hippocampal long-term potentiation

Neuroreport. 1993 Jun;4(6):712-4. doi: 10.1097/00001756-199306000-00028.


The possible involvement of cAMP-dependent protein kinase A (PKA) in mechanisms of long-term potentiation of the Schaffer collateral-commissural input of rat CA1 neurones was investigated using several inhibitors in vitro. If 10 microM H-8, 100 nM KT5720 or 50 microM Rp-cAMPs was applied to the bath before a triple 100 Hz/0.5 s tetanization, post-tetanic and short-term potentiation developed almost normally. However, from about 3 h after tetanization the long-term potentiation (LTP) of the field-EPSP declined with respect to the control in an irreversible manner. These data suggest that besides protein kinase C the synergistic activation of PKA is necessary for the maintenance of LTP.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carbazoles*
  • Electric Stimulation
  • Hippocampus / drug effects*
  • Hippocampus / physiology
  • In Vitro Techniques
  • Indoles / pharmacology
  • Isoquinolines / pharmacology
  • Male
  • Neuronal Plasticity / drug effects*
  • Phosphorylation
  • Protein Kinase C / antagonists & inhibitors
  • Protein Kinase Inhibitors*
  • Pyrroles / pharmacology
  • Rats
  • Rats, Wistar
  • Synapses / physiology


  • Carbazoles
  • Indoles
  • Isoquinolines
  • Protein Kinase Inhibitors
  • Pyrroles
  • KT 5720
  • N-(2-(methylamino)ethyl)-5-isoquinolinesulfonamide
  • Protein Kinase C