In order for long-term potentiation (LTP) to occur, there must be stimulation of NMDA receptors, which causes AMPA receptors to be inserted postsynaptically. PI3K binds to AMPA receptors in a conserved region to orient the receptors in the membrane, specifically at the GluR subunit. PI3K activity increases in response to calcium ions and CaM. Additionally, AKT localizes PtdIns-3Ps in the post synapse, which recruits docking proteins such as tSNARE and Vam7. This directly leads to the docking of AMPA in the post synapse.  mTOR activated p70S6K and inactivated 4EBP1 which changes gene expression to allow LTP to occur. Long-term fear conditioning training was affected in rats but there was no effect in short term conditioning. Specifically, amygdala fear conditioning was lost. This is a type of trace conditioning which is a form of learning that requires association of a conditioned stimulus with an unconditioned stimulus. This effect was lost in PI3K knockdowns and increased in PI3K overexpressions.