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Electron-donating nucleophilic compounds activate TRPA1 ion channels in fruit flies and mosquitoes, but not humans, making TRPA1 a promising target for insect repellants.

Drosophila experience two hunger states, one driven by need and the other by pleasure, which arise from unique neural substrates.

Fruit flies have special neurons in their pharynx with ionotropic receptors to prevent consuming too much salt, which was confirmed using a variety of behavioral and physiological assays.

Unlike other taste modalities, the Drosophila taste system encodes salt taste combinatorially across multiple sensory neuron classes, which combine to produce behavioural valence and plasticity.

Fruit flies can taste and avoid food contaminated with a bacterial toxin using the same channel protein that functions in humans as sensor of noxious chemical stimuli.

Taste-dependent satiation, which induces proper cessation of feeding in mammals as well as insects, is weakened by sugar-diet-driven taste impairment in the fruit fly.

Bitter-sensing cells across different organs of the fruit fly activate overlapping neural pathways in the brain to regulate a common set of aversive behaviors.

A split-GAL4 collection provides precise genetic targeting of 138 neuronal cell types in the subesophageal zone of adult Drosophila melanogaster.

Insect specific olfactory receptors are not an adaptation to a terrestrial insect lifestyle, but evolved later in insect evolution.

Genetic, behavioral, and biochemical evidence reveals that the Drosophila TRPγ channel is required in neuroendocrine cells for the starvation-induced switch in preference to less palatable but more nutritive food.