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 α, β, ϵ PKC showed enhanced translocation, while postsynaptic γ 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.
