Complexins (Cplxs) are essential SNARE complex regulators controlling the fusogenicity of primed synaptic vesicles (SV). Altered Cplx expression has been linked to psychiatric and neurological disorders. Multiple lines of research show that Cplxs promote synchronous action potential (AP)-triggered SV fusion. In some preparations, such as the murine calyx of Held, loss of Cplxs leads to an upregulation of asynchronous SV fusion events suggesting that Cplx can also exert a ‘fusion clamp’-like function. Here, we studied functional consequences of genetic Cplx1 ablation at nearly mature mouse calyx of Held synapses which predominantly expresses this Cplx isoform in their calyceal terminals. At this synapse, loss of Cplx1 reduces synaptic strength and promotes asynchronous fusion events following trains of presynaptic action potentials (APs). Surprisingly, the rate of delayed fusion events was completely unaltered in synapses lacking both Cplx1 as well as Synaptotagmin 7 indicating that Syt7 is dispensable for this kind of asynchronous release. Instead, we propose that aberrant delayed SV fusion results form an accumulation of SV in a meta-stable state during the pool replenishment process. While the dwell time of primed SVs in this meta-stable state is very short in the presence of Cplx1, it is considerable prolong after genetic loss of Cplx1 which causes SV to be more prone to premature release. We implemented a simple kinetic model of the SV priming process featuring a Cplx1-dependent transition from pre-primed to fully-primed state which allows one to replicate both amplitude and time course of delayed fusion in the presence and absence of Cplx1.