Differential translocation of protein kinase C isozymes in rats characterized by a chronic lack of LTP induction and cognitive impairment.

The translocation of protein kinase C isozymes was investigated in an animal model of cognitive deficit and lack of induction of long-term potentiation (LTP). In MAM rats, presynaptic alpha, beta, epsilon PKC showed enhanced translocation, while postsynaptic gamma PKC displayed decreased translocation when compared to control levels. This imbalance of PKC isozyme translocation between the pre- and post-synaptic compartment might therefore represent a possible molecular cause for the lack of synaptic plasticity observed in these animals.