Genetic mosaic analysis revealed that ennui is necessary cell autonomously in muscle fibers for normal synaptic localization of acetylcholine receptors.
Clinically, its venom contains presynaptic and postsynaptic neurotoxins, which generally affect the nerve endings near the synaptic cleft of the brain.
When chloride enters the nerve cell, the cell membrane potential hyperpolarizes thereby inhibiting depolarization, or reduction in the firing rate of the post-synaptic nerve cell.
Additionally, by disrupting proper synaptic function through nicotine exposure, the overall circuit may become less sensitive and responsive to stimuli, resulting in compensatory developmental plasticity.