 At a molecular level, the net result of the activation of this pathway, is the spontaneous stimulation of inhibitory PF1-like neuropeptide release (this is suspected due to Emodepside's inhibition of acetylcholine-elicited muscle contraction requiring both calcium ions and extracellular potassium ions, similar to the action of PF1/PF2).Although in experiments on synaptosomes, α-LTX triggered non-calcium dependent exocytosis of vesicles containing acetylcholine, glutamate and GABA, both glutamate and GABA have been ruled out as the sole neurotransmitters responsible for emodepside's action) which then acts on the post-synaptic membrane (i.e.the pharyngeal/muscle membrane) of the nematode, having an inhibitory effect thereby either inducing paralysis or inhibiting pharyngeal pumping, both of which ultimately result in the death of the organism.