Synaptic vesicle glycoprotein 2 (SV2) and ganglioside complex (SV2 (including isoforms SV2A, SV2B, SV2C) and gangliosides)

Synaptic vesicle glycoprotein 2 (SV2) is a family of 12-transmembrane glycoproteins (SV2A, SV2B, SV2C) that reside on synaptic vesicles in presynaptic nerve terminals, notably in cholinergic neurons[7][6]. They are critical for the regulation of neurotransmitter release, vesicle trafficking, and calcium sensitivity of synaptic vesicle exocytosis[7][6]. SV2 proteins serve as receptors for several serotypes of botulinum neurotoxins (BoNT/A, E, D, F), enabling toxin entry into neurons in concert with membrane gangliosides in a "double-receptor" mechanism[1][2][3][4]. Gangliosides, especially polysialogangliosides like GT1b, are membrane glycolipids that cooperate with SV2 to mediate efficient binding and uptake of neurotoxins[2][5]. SV2A is the therapeutic target of antiepileptic drugs like levetiracetam and brivaracetam[7]. Disruption of SV2 function is associated with neurological dysfunction, and abnormal SV2 or ganglioside roles are implicated in epilepsy, botulism, and neurodegenerative diseases[7][6]. Note: While “SV2 and gangliosides” together form a therapeutic *target complex* for botulinum neurotoxin entry, “SV2” alone is the canonical therapeutic target for drugs like levetiracetam. Since the original entity combines two disparate molecular types (a glycoprotein family and glycolipids), this may not map cleanly to any single standardized target nomenclature, so is_incorrect=true.

Other names

SV2 (family: SV2A, SV2B, SV2C)Synaptic vesicle protein 2Synaptic vesicle glycoprotein 2Synaptic vesicle protein 2A, 2B, 2CPolysialogangliosides (for gangliosides)Ganglioside GT1b (specific for some interactions)

Levetiracetam: modulation of neurotransmitter release via binding to SV2A Botulinum neurotoxins: toxin entry into cholinergic nerve terminals via dual receptor (SV2 glycoprotein luminal domain + gangliosides), leading to synaptic blockade Brivaracetam: similar to levetiracetam, SV2A binding and neurotransmitter release modulation