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Kinetic modelling was combined with non\u2010negative tensor factorization (NTF) to separate changes in synaptic vesicle (SV) priming kinetics from those in SV fusion probability (\n p<\/jats:italic>\n fu<\/jats:sub>\n sion<\/jats:sub>\n ). Heterogeneous synaptic strength and STP under control conditions can be fully accounted for by assuming a uniform\n p<\/jats:italic>\n fusion<\/jats:sub>\n among calyx synapses yet profound synapse\u2010to\u2010synapse variation in the resting equilibrium of SVs in functionally distinct priming states. Although synaptic potentiation induced by either elevated resting [Ca\n 2+<\/jats:sup>\n ]\n i<\/jats:sub>\n , elevated external [Ca\n 2+<\/jats:sup>\n ] or stimulation of the diacylglycerol (DAG) signalling pathway leads to seemingly similar changes, that is, stronger synapses with less facilitation and more pronounced depression, the underlying mechanisms are different. Specifically, synaptic potentiation induced by the DAG mimetic and Munc13\/PKC activator phorbol 12,13\u2010dibutyrate (PDBu) only moderately enhances\n p<\/jats:italic>\n fusion<\/jats:sub>\n but strongly increases the abundance of fusion\u2010competent maturely primed SVs, demonstrating that the dynamic equilibrium of differentially primed SVs critically determines synaptic strength and STP. Activation of the DAG pathway not only stimulates priming at resting [Ca\n 2+<\/jats:sup>\n ]\n i<\/jats:sub>\n but further promotes SV pool replenishment at elevated [Ca\n 2+<\/jats:sup>\n ]\n i<\/jats:sub>\n following pool\u2010depleting stimulus trains. A two\u2010step priming and fusion scheme which recapitulates the sequential build\u2010up of the molecular SV fusion machinery is capable of reproducing experimentally induced changes in synaptic strength and STP in numerical simulations with a small number of plausible model parameter changes.\n \n \n image<\/jats:alt-text>\n <\/jats:graphic>\n <\/jats:boxed-text>\n <\/jats:p>\n <\/jats:sec>\n \n Key points<\/jats:title>\n \n \n \n A relatively simple two\u2010step synaptic vesicle (SV) priming and fusion scheme is capable of reproducing experimentally induced changes in synaptic strength and short\u2010term plasticity with a small number of plausible parameter changes.<\/jats:p>\n <\/jats:list-item>\n \n The combination of non\u2010negative tensor factorization (NTF)\u2010decomposition analysis and state modelling allows one to separate experimentally induced changes in SV priming kinetics from those in SV fusion probability.<\/jats:p>\n <\/jats:list-item>\n \n \n A relatively low sensitivity of the SV priming equilibrium to changes in resting [Ca\n 2+<\/jats:sup>\n ]\n i<\/jats:sub>\n suggests that the amplitude of the \u2018effective\u2019 action potential (AP)\u2010induced Ca\n 2+<\/jats:sup>\n transient is quite large, likely representing contributions of global and local Ca\n 2+<\/jats:sup>\n signals.\n <\/jats:p>\n <\/jats:list-item>\n \n Enhanced synaptic strength and stronger depression after stimulation of the diacylglycerol (DAG) signalling pathway is primarily caused by enhanced SV priming, leading to increased abundance of maturely primed SVs at rest with comparably small changes in SV fusion probability.<\/jats:p>\n <\/jats:list-item>\n \n \n Application of DAG mimetics enhances the Ca\n 2+<\/jats:sup>\n \u2010dependent acceleration of SV priming causing a faster recovery of synaptic strength after pool\u2010depleting stimuli.\n <\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n 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