Figure 2

Proposed role of aPKCs in synaptic plasticity: At most CNS synapses, strong synaptic input leads to an activation of PI3K signaling and PDK1 activation thereby (1) thereby leading to mTORC1 activation. Engagement of the mTORC1 pathway leads to an increase in translation at or near synaptic sites (2). Because aPKCs mRNAs localize to dendritic and/or synaptic sites, this mTORC1 activation is capable of stimulating nascent synthesis of aPKCs, especially PKMζ (3). Because PDK1 is also activated, this strong synaptic input is linked to increased synthesis and phosphorylation of aPKCs. This enhancement of aPKC number and/or activity at synaptic sites is then linked to increased trafficking of AMPARs to the postsynaptic density (PSD), thereby promoting LTP maintenance.