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Fig. 2 | Molecular Brain

Fig. 2

From: A two-compartment model of synaptic computation and plasticity

Fig. 2

Pre- and postsynaptic plasticity are mechanistically distinct. a Conventional model of NMDAR-dependent synaptic plasticity at central synapses. Hebbian activity is sensed by postsynaptic NMDARs and translated into a postsynaptic influx of Ca2+. This leads to the exo- or endocytosis of AMPARs, which depends on the magnitude of Ca2+ influx. Additionally, NMDAR-dependent Ca2+ influx is conventionally thought to trigger the synthesis and release of retrograde signals such as nitric oxide (NO), which then modulates plasticity at the presynaptic terminal. b Novel model of presynaptic plasticity [53]. At the hippocampal Schaffer collateral-CA1 synapse, changes in Pr are driven by two parallel molecular mechanisms that are independent of postsynaptic NMDARs: 1) Presynaptic LTP, which is induced by Hebbian activity, involving the causal pairing of presynaptic action potentials and strong postsynaptic depolarisation. Postsynaptic depolarisation, in the form of dendritic spikes or back-propagating action potentials, driven by cooperative synaptic activity, triggers the synthesis and release of NO in dendritic branches [53]. At the presynaptic terminal, NO can increase Pr but only when presynaptic activity precedes its release. Such timing requirements are likely mediated by an as yet unidentified Hebbian coincidence detector in the presynaptic terminal. 2) Presynaptic LTD, which is triggered by glutamate release via the activation of presynaptic NMDARs. Accordingly, presynaptic LTP is preferentially induced at synapses releasing little or no glutamate during Hebbian activity

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