recruitment of calciumpermeable ampa receptors during synaptic potentiation is regulated by camkinase i ca2permeable ampa receptors cpampars at central glutamatergic synapses are of special interest because of their unique biophysical and signaling properties that contribute to synaptic plasticity and their roles in multiple neuropathologies however intracellular signaling pathways that recruit synaptic cpampars are unknown and involvement of cpampars in hippocampal region ca1 synaptic plasticity is controversial here we report that intracellular infusion of active camkinase i camki into cultured hippocampal neurons enhances miniature epsc amplitude because of recruitment of cpampars likely from an extrasynaptic pool the ability of camki which regulates the actin cytoskeleton to recruit synaptic cpampars was blocked by inhibiting actin polymerization with latrunculin a camk regulation of cpampars was also confirmed in hippocampal slices ca1 longterm potentiation ltp after theta bursts but not highfrequency tetani produced a rapid transient expression of synaptic cpampars that facilitated ltp this component of tbs ltp was blocked by inhibition of camkinase kinase camkk the upstream activator of camki our calculations show that adding cpampars numbering 5 of existing synaptic ampars is sufficient to account for the potentiation observed in ltp thus synaptic expression of cpampars is a very efficient mechanism for rapid enhancement of synaptic strength that depends on camkkcamki signaling actin dynamics and the pattern of synaptic activity used to induce ca1 ltp