Scientific article

Protein kinase C activity is not responsible for the expression of long-term potentiation in hippocampus

Publication date1990

Long-term potentiation (LTP) in hippocampus has been proposed to result from a tonic activation of protein kinase C. This hypothesis predicts that stimulation of the kinase would produce a smaller change in response size on potentiated versus control pathways and, conversely, that inhibition of the kinase would reduce potentiated inputs to a greater degree than control responses. We tested these predictions using phorbol esters to activate and using the antagonist H-7 to inhibit protein kinase C; we found that the actions of these drugs on synaptic transmission were not affected by prior induction of LTP. Both compounds, however, significantly decreased the contribution of N-methyl-D-aspartate receptors to synaptic potentials, a result that accounts for the suppressive effects of these compounds on LTP formation. Thus protein kinase C is probably not involved in the expression of LTP but may play a role in the receptor-mediated events participating in its induction.

  • Animals
  • Hippocampus/ enzymology
  • Isoquinolines/pharmacology
  • Membrane Potentials/drug effects
  • Neuronal Plasticity/ physiology
  • Phorbol Esters/pharmacology
  • Piperazines/pharmacology
  • Protein Kinase C/antagonists & inhibitors/ physiology
  • Rats
  • Receptors, N-Methyl-D-Aspartate
  • Receptors, Neurotransmitter/physiology
  • Synaptic Transmission/drug effects/physiology
  • Time Factors
Citation (ISO format)
MULLER, Dominique et al. Protein kinase C activity is not responsible for the expression of long-term potentiation in hippocampus. In: Proceedings of the National Academy of Sciences of the United States of America, 1990, vol. 87, n° 11, p. 4073–4077.
Updates (1)
ISSN of the journal0027-8424

Technical informations

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