Long-term potentiation (LTP) can have an early phase constituting a transient increase in synaptic strength, and a late phase sustaining this increase. The synaptic tagging and capture hypothesis states that the late phase occurs if the stimulus leads to a transient ‘synaptic tag’ along with plasticity-related protein (PRP) synthesis. If both are present, the post synaptic density (PSD) remodels, giving rise to long-lasting changes in the synaptic weight. With computational modelling, we test the hypothesis that actin dynamics in interaction with spine geometry acts as a synaptic tag.Actin dynamics is constituted by several actin binding proteins that carry out filament branching, capping, severing and crosslinking which are modulated during LTP. We first study the dynamic (not crosslinked) actin pool during LTP and find that the enhanced actin activity only persists during the modulation. Hence it cannot serve as a ‘tag’ on its own.We then add a stable actin pool (crosslinked) and couple with a 3d model for the spine membrane, which is determined through forces from actin and the counteracting membrane forces. We show that, when the PSD is not remodelled (no PRPs), LTP-like perturbations of the stable pool and total spine volume are retained on the time-scale of the synaptic tag, but ultimately decay to a state determined by the PSD. When PSD remodels, it adapts to the perturbed spine geometry.Taken together, our model provides proof-of-principle that the interaction of actin dynamics and spine geometry acts as a synaptic tag.