Dendritic spines at excitatory synapses undergo rapid, actin-dependent shap
e changes which may contribute to plasticity in brain circuits. Here we sho
w that actin dynamics in spines are potently inhibited by activation of eit
her AMPA or NMDA subtype glutamate receptors. Activation of either receptor
type inhibited actin-based protrusive activity from the spine head. This b
lockade of motility caused spines to round up so that spine morphology beca
me both more stable and more regular. Inhibition of spine motility by AMPA
receptors was dependent on postsynaptic membrane depolarization and influx
of Ca2+ through voltage-activated channels. In combination with previous st
udies, our results suggest a two-step process in which spines initially for
med in response to NMDA receptor activation are subsequently stabilized by
AMPA receptors.