Persistent activation of protein kinase C during the development of long-term facilitation in Aplysia.

We investigated activation of the two major neuronal protein kinase C (PKC) isoforms in Aplysia, Ca(2+)-activated Apl I and Ca(2+)-independent Apl II, during the induction and maintenance of behavioral sensitization of Aplysia defensive reflexes. Activation of PKC occurred during the training stimulus and persisted for at least 2 hr thereafter but was not maintained for 24 hr. The persistent activation required protein synthesis and was blocked by cyproheptidine, an agent that also blocked the initial activation of PKC. Persistent activation involved both an increase in membrane-associated Apl I and an increase in an autonomous kinase activity that may be related to a post-translational modification of Apl II. These results are consistent with the hypothesis that in addition to its role in producing the presynaptic facilitation of mechanosensory-motor neuron synapses that underlie short-term facilitation, PKC is needed for maintaining synaptic changes in an intermediate period that precedes the modifications accompanying consolidation of memory.