Alterations of potassium channels has recently been implicated in the inhibitory effects of ethanol. Davies, McIntire, et al. studied effects of ethanol on the round worm C. elegans, believing that alcohol-mediated inhibition of neural activity would be conserved across species. Previously it has been shown that the dose-effect curves for behavioral changes is similar for both invertebrates and vertebrates. Ethanol seems to affect many different proteins that would lead to synaptic inhibition, including GABA and glutamate channels and potassium channels. Many different gene products (dopamine D4 receptors, protein kinase C) are associated with increased sensitivity while others (nitric oxide synthase, dopamine D2) are associated with ethanol resistance. These changes suggest the complex pathways are involved in ethanol effects but don't isolate a specific target for its effects.
When C. elegans were exposed to ethanol for brief time periods, ethanol levels rose to values similar to levels seen in intoxicated drivers (0.1%). They isolated mutants that were resistant to ethanol effects (changes in movement and egg-laying behavior). These mutants affected a single gene, slo-1, homologous to the the slowpoke gene in drosophila. The gene in both organisms encoded a BK potassium channel, whose normal function is to repolarize neural membranes. Mutant strains, when transformed with slo-1+ regained ethanol sensitivity. Ethanol appears to directly activate the channel. This would lead to efflux of potassium ions from the worm, hyperpolarizing the neural cells, leading to inhibition of neural activity. Effects in C. elegans were observed at physiologically relevant ethanol, ranging from those that produce euphoria to sedation in humans.