 As IP3 receptors have sparse or little distribution throughout the pharyngeal nervous system of C.elegans (one of the tissues where LAT-1 agonists such as α-LTX and emodepside have their most predominant effects) and β-phorbel esters (which mimic the effects of DAG) have been shown to have a stimulatory action on synaptic transmission, it has been concluded that it is the DAG component of the cascade that regulates neurotransmitter release.Indeed, in C.elegans DAG regulates UNC-13, a plasma-membrane associated protein critical for vesicle-mediated neurotransmitter release and mutational studies have shown that two UNC-13 reduction of function mutants show resistance to emodepside, observations supporting this hypothesized mechanism of action.The mechanism by which activation of UNC-13 results in neurotransmitter release (the ultimate result of latrophilin activation) is through interaction with the synaptosomal membrane protein syntaxin, with UNC-13 binding to the N-terminus of syntaxin and promoting the switch from the closed form of syntaxin (which is incompatible with SNARE complex synaptobrevin, SNAP-25 and syntaxin formation) to its open formation so that SNARE complex formation can be achieved, thereby allowing vesicle fusion and release to take place.