Classical synaptic long-term potentiation (LTP) requires NMDA receptor (NMDAR) activation, which drives AMPA receptor (AMPAR) insertion into the postsynaptic membrane. Here, activation of kainate receptors (KARs) in rat CA1 neurons triggered an increase in postsynaptic AMPAR surface expression and potentiated AMPAR-mediated CA1 excitatory postsynaptic responses. These changes were independent of NMDAR activation and required KAR-mediated metabotropic signalling via G-protein-dependent increases in intracellular Ca2+, protein kinase C activation, and increased recruitment of recycling endosomes.