 These subunits group together to form high conductance BK-type channels that are gated by both membrane potential and intracellular calcium levels (this calcium ion sensing ability is accommodated by an intracellular tail region on Slo-like subunits that form a calcium ion binding motif consisting of a run of conserved aspartate residues, termed a “calcium bowl”), with their physiological role being to regulate the excitability of neurons and muscle fibres, through the way in which they participate in action potential repolariziation (with potassium ion efflux being used to repolarize the cell following depolarization).The presumable effect that emodepside interaction with these channels would exert on the neuron would be to activate the channel causing potassium ion efflux, hyper-polarization and subsequent inhibition of excitatory neurotransmitter effect (acetylcholine if acting at the neuromuscular junction), having an inhibitory effect on synaptic transmission, the production of postsynaptic action potentials and ultimately muscle contraction (manifesting itself as paralysis or reduced pharyngeal pumping).Which out of Latrophilin receptors and BK-potassium channels is emodepside's primary site of action remains to be completely deduced.