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K+ channels are key regulators of cellular excitability. Mutations that activate K+ channels can lower cellular excitability, whereas those that inhibit K+ channels may increase excitability. We show that the Caenorhabditis elegansegl-2 gene encodes an eag K+ channel and that a gain-of-function mutation in egl-2 blocks excitation in neurons and muscles by causing the channel to open at inappropriately negative voltages. Tricyclic antidepressants reverseegl-2(gf) mutant phenotypes, suggesting that EGL-2 is a tricyclic target. We verified this by showing that EGL-2 currents are inhibited by imipramine. Similar inhibition is observed with the mouse homolog MEAG, suggesting that inhibition of EAG-like channels may mediate some clinical side effects of this class of antidepressants.

Block of an ether-a-go-go-Like K+Channel by Imipramine Rescuesegl-2Excitation Defects inCaenorhabditis elegans

Block of an ether-a-go-go-Like K⁺Channel by Imipramine Rescuesegl-2Excitation Defects inCaenorhabditis elegans