We review biophysical models of synaptic plasticity, with a focus on spike-timing dependent plasticity (STDP). The common property of the discussed models is that synaptic changes depend on the dynamics of the intracellular calcium concentration, which itself depends on pre- and postsynaptic activity. We start by discussing simple models in which plasticity changes are based directly on calcium amplitude and dynamics. We then consider models in which dynamic intracellular signaling cascades form the link between the calcium dynamics and the plasticity changes. Both mechanisms of induction of STDP (through the ability of pre/postsynaptic spikes to evoke changes in the state of the synapse) and of maintenance of the evoked changes (through bistability) are discussed.
Keywords: CaMKII; STDP; biophysical models; bistability; calcium control hypothesis; induction; maintenance; protein signaling cascade.