Long-term potentiation, protein kinase C, and glutamate receptors.
Among the various molecular events that have been proposed to contribute to the mechanisms of long-term potentiation (LTP), one of the most cited possibilities has been the activation of protein kinase C (PKC). Here we review various aspects of the cellular actions of PKC activation and inhibition, with special emphasis on the effects of the kinase on synaptic transmission and the N-methyl-D-aspartate (NMDA) and non-NMDA receptor-mediated components of synaptic responses. We discuss the implications of these effects for interpretations of the role of PKC in the mechanisms of LTP induction and maintenance.
Muller
D
D
Department of Pharmacology, Centre Medical Universitaire, Geneva, Switzerland.
Buchs
P A
PA
Stoppini
L
L
Boddeke
H
H
D000818:Animals; D004789:Enzyme Activation; D006624:Hippocampus / Q000502:physiology*; D006801:Humans; D008568:Memory / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D010703:Phorbol Esters / Q000494:pharmacology; D011493:Protein Kinase C / Q000502:physiology*; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology; D017981:Receptors, Neurotransmitter / Q000502:physiology*; D015398:Signal Transduction; D009435:Synaptic Transmission / Q000502:physiology*
D010703:Phorbol Esters; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; D011493:Protein Kinase C