calcium transients in spines are a key trigger for synaptic plasticity. nmda receptors, which have a high permeability for calcium, only conduct ions if the membrane potential is suffiently depolarized. the amount of calcium entering a spine during synaptic activity therefore depends on the depolarization of the spine head. evidence from calcium imaging experiments (two-photon microscopy) and from compartmental modelling indicates that spines with high resistance necks experience larger calcium transients during synaptic activity.