Abstract
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.
Highlights
Long-term synaptic modifications have long been postulated to occur in response to the simultaneous activation of both pre- and postsynaptic neurons (Hebb, 1949)
In the hippocampus (Levy and Steward, 1983; Gustafsson et al, 1987; Magee and Johnston, 1997; Bi and Poo, 1998), the Xenopus tectum (Zhang et al, 1998), the visual cortex (Markram et al, 1997; Sjöström et al.,2001),and the somatosensory cortex (Feldman,2000) an EPSP occurring prior to the backpropagating action potential evokes long-term potentiation (LTP), and the anti-causal order, i.e., the EPSP occurs after the postsynaptic neuron spiked, leads to long-term depression (LTD)
Since the early spike-timing dependent plasticity (STDP) experiments, numerous studies in different brain regions and under varying experimental conditions have revealed a plethora of STDP shapes
Summary
Long-term synaptic modifications have long been postulated to occur in response to the simultaneous activation of both pre- and postsynaptic neurons (Hebb, 1949). Calcineurin Experimental results indicate that the sign of hippocampal synaptic plasticity is regulated by the balance between protein phosphorylation and dephosphorylation mediated by PKA and calcineurin, respectively Consistent with this idea, overexpression of calcium/ calmodulin-dependent calcineurin in the forebrain of transgenic mice is found to impair an intermediate and PKA-dependent phase of LTP, as well as the transition from short- to long-term memory and memory retrieval (Mansuy et al, 1998; Winder et al, 1998). Evidence for the role of I1 as a point of convergence is: (i) Hippocampal LTD induction involves calcium/calmodulin-dependent calcineurin dephosphorylating I1 (Mulkey et al, 1994), (ii) Synaptic stimulation that induces cAMP-dependent LTP raises the amount of phosphorylated I1 in the CA1 region (Blitzer et al, 1998) This increase is dependent on PKA activity since it is blocked by PKA inhibitors. In both models, such high calcium transients boost phos. inhibitor 1 concentration (μM)
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