Ephaptic coupling is a unique way physically adjacent neurons can influence one another's activity that, without an underlying molecular mechanism, could easily be considered a form of electrical interference rather than a genuine contributor to information processing. Here, we show the hyperpolarization-activated cyclic nucleotide-gated (HCN) channel unilateralizes the ephaptic inhibition of Drosophila gustatory receptor neurons (GRNs). HCN in sweet-sensing GRNs (sGRNs) allows sweetness to dominate bitterness. Simultaneously, HCN, throttling sGRNs in sugar-rich environments, enhances bitter-sensing GRN sensitivity to allow for uncompromised aversion to potentially toxic bitter substances. Thus, ephaptic inhibition can be genetically programmed and subjected to natural selection. This implies ephaptic coding arose to meet a physiologic need and may provide mechanistic insights into the well-known but enigmatic phenomenon of sweet-dependent taste suppression in humans.

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