Molecular control limiting sensitivity of sweet taste neurons in <i>Drosophila</i>.

Abstract

To assess the biological value of environmental stimuli, animals' sensory systems must accurately decode both the identities and the intensities of these stimuli. While much is known about the mechanism by which sensory neurons detect the identities of stimuli, less is known about the mechanism that controls how sensory neurons respond appropriately to different intensities of stimuli. The ionotropic receptor <i>IR76b</i> has been shown to be expressed in different <i>Drosophila</i> chemosensory neurons for sensing a variety of chemicals. Here, we show that <i>IR76b</i> plays an unexpected role in lowering the sensitivity of <i>Drosophila</i> sweet taste neurons. First, <i>IR76b</i> mutants exhibited clear behavioral responses to sucrose and acetic acid (AA) at concentrations that were too low to trigger observable behavioral responses from WT animals. Second, <i>IR76b</i> is expressed in many sweet neurons on the labellum, and these neurons responded to both sucrose and AA. Removing <i>IR76b</i> from the sweet neurons increased their neuronal responses as well as animals' behavioral responses to sucrose and AA. Conversely, overexpressing <i>IR76b</i> in the sweet neurons decreased their neuronal as well as animals' behavioral responses to sucrose and AA. Last, <i>IR76b</i>'s response-lowering ability has specificity: <i>IR76b</i> mutants and WT showed comparable responses to capsaicin when the mammalian capsaicin receptor <i>VR1</i> was ectopically expressed in their sweet neurons. Our findings suggest that sensitivity of <i>Drosophila</i> sweet neurons to their endogenous ligands is actively limited by <i>IR76b</i> and uncover a potential molecular target by which contexts can modulate sensitivity of sweet neurons.