Another possible model for fusion pore formation is the protein-lined pore theory.  In this model, after activation of synaptotagmin by calcium, several SNARE complexes come together to form a ring structure, with synaptobrevin forming the pore in the vesicle membrane and Syntaxin forming the pore in the cell membrane.  As the initial pore expands it incorporates lipids from both bilayers, eventually resulting in complete fusion of the two membranes.  The SNARE complex has a much more active role in the protein-lined pore theory; because the pore consists initially entirely of SNARE proteins, the pore is easily able to undergo intercellular regulation, making fluctuation and "kiss-and-run" mechanisms easily attainable.
A protein-lined pore perfectly meets all the observed requirements of the early fusion pore, and while some data does support this theory, sufficient data does not exist to pronounce it the primary method of fusion. A protein-lined pore requires at least five copies of the SNARE complex while fusion has been observed with as few as two.
In both theories the function of the SNARE complex remains largely unchanged, and the entire SNARE complex is necessary to initiate fusion.  It has, however, been proven that in vitro Syntaxin per se is sufficient to drive spontaneous calcium independent fusion of synaptic vesicles containing v-SNAREs. This suggests that in Ca-dependent neuronal exocytosis synaptotagmin is a dual regulator, in absence of Ca ions to inhibit SNARE dynamics, while in presence of Ca ions to act as agonist in the membrane fusion process.