An increasing body of evidence indicates that PKA is important for synaptic plasticity in the hippocampus. AKAP150 is a PKA anchoring protein that is involved in the regulation of AMPA-type glutamate receptors. Extracellular recordings from the CA1 region of the Schaffer collateral pathway in the hippocampus did not reveal any changes in either LTP or LTD in AKAP150 knockout mice compared to wild type mice. To circumvent potential compensatory mechanisms by other AKAPs in the knock-out mice, mice with a targeted deletion of the C-terminal 36 residues of AKAP150, which constitute the PKA binding site, were generated. In preliminary experiments a reduction in both, LTP and LTD, in the deletion mutant mice suggests that AKAP150 is involved in synaptic plasticity of hippocampus. My current project is to investigate the synaptic plasticity and the possible underlying mechanisms in the AKAP150 mutant mice.