The role of actin filaments in synaptic function has been studied in the CA1 region of the rat hippocampal slice. Bath application (2 hr) of the actin polymerization inhibitor latrunculin B did not substantially affect the shape of dendrites or spines. However, this and other drugs that affect actin did affect synaptic function. Bath-applied latrunculin B reduced the synaptic response. Several lines of evidence indicate that a component of this effect is presynaptic. To specifically test for a postsynaptic role for actin, latrunculin B or phalloidin, an actin filament stabilizer, was perfused into the postsynaptic neuron. The magnitude of long-term potentiation (LTP) was decreased at times when baseline transmission was not yet affected. Longer applications produced a decrease in baseline AMPA receptor (AMPAR)-mediated transmission. The magnitude of the NMDA receptor-mediated transmission was unaffected, indicating a specific effect on the AMPAR. These results suggest that postsynaptic actin filaments are involved in a dynamic process required to maintain AMPAR-mediated transmission and to enhance it during LTP.