Plays a role in the control of regulated secretion in neural and endocrine cells, enhancing selectively low-frequency neurotransmission. Positively regulates vesicle fusion by maintaining the readily releasable pool of secretory vesicles. (Microbial infection) Receptor for C.botulinum neurotoxin type A (BoNT/A, botA); the toxin binds Sv2c via extracellular loop 4 (PubMed:16543415). (Microbial infection) Possible receptor for C.botulinum neurotoxin type D (BoNT/D, botD) (PubMed:21483489). Interacts with SYT1 in a calcium-dependent manner. (Microbial infection) Interacts with C.botulinum neurotoxin type A (BoNT/A, botA). (Microbial infection) Interacts with C.botulinum neurotoxin type D (BoNT/D, botD). Enriched in small synaptic vesicles and adrenal microsomes, not present in chromaffin granules. Associated with both insulin granules and synaptic-like microvesicles in insulin-secreting cells of the pancreas. Expressed in specific subsets of conventional synapses in the retina (at protein level) (PubMed:12687700). Expressed in diaphragm motor nerve terminals (at protein level) (PubMed:16543415). Expressed in a subset of hippocampus neurons (at protein level) (PubMed:18815274, PubMed:21483489). Expressed during synaptogenesis in the retina (at protein level). Up-regulated upon Sv2a depletion. N-glycosylated. Small interfering RNA knockdown of the protein in Neuro-2a cells (which only express this SV2 protein) prevents uptake of C.botulinum neurotoxin type A (BoNT/A, botA); uptake is restored by expression of rat SV2A or SV2B (PubMed:16543415). Belongs to the major facilitator superfamily. The use of this protein as a coreceptor for C.botulinum type D (BoNT/D, botD) is controversial. In double SV2A/SV2B knockout mice BoNT/D does not degrade its synaptobrevin target; introducing SV2A, SV2B or SV2C restores target cleavage (PubMed:21483489). However another group does not find a convincing interaction with SV2 (PubMed:21632541). Extended N-terminus.