Dendritic spines—the main sites of excitatory synaptic contacts in the CNS—have been in the spotlight recently. Their curious motility has been linked to synapse formation as well as plasticity in response to sensory experience. Now, Matus and colleagues (pages 887–894, this issue) have directly addressed the mechanism by which neural activity and spine motility may be linked. The authors made time-lapse videos of spine motility in GFP-actin transfected hippocampal neurons as well as slice cultures from transgenic mice expressing GFP-tagged actin. A major finding was that actin dynamics are rapidly and reversibly inhibited following activation of AMPA receptors—spines became more stable and assumed a more regular appearance. Furthermore, inhibition of motility via AMPA receptors required postsynaptic membrane depolarization and the influx of calcium. In combination with previous work, the results suggest that spines initially formed by NMDA receptor activation are subsequently stabilized by AMPA receptors. Although the results may seem paradoxical because the quite different processes of spine formation and stabilization both require the influx of calcium, the authors point out that there are interesting parallels with growth cone motility, where calcium activation at different stages of synapse formation can have opposite effects.