Synaptic plasticity, the activity-dependent change in the strength of neuronal connections, is a proposed cellular mechanism of memory storage that requires protein kinases such as cAMP-dependent protein kinase (PKA). Spatial compartmentalization of PKA via binding to A-Kinase Anchoring Proteins (AKAPs) is thought to contribute to the specificity of the PKA signaling pathway in effecting downstream events. Because the regulation of specificity is crucial to signal transduction pathways, we tested the hypothesis that mislocalizing PKA by Ht31, an inhibitor of PKA anchoring, would alter PKA-dependent behavioral and physiological processes. Mice that inducibly express Ht31 in forebrain neurons display alterations in hippocampal function as assessed by impairments in the spatial version of the Morris Water maze for example (Nie and Abel, SFN 2002, 2003). Expression of Ht31 also disrupts certain AKAP complexes that contain PKA and impairs a PKA-dependent form of hippocampal L-LTP (McDonough et al., SFN 2004). H...