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Finding food sources is essential for survival. Insects detect nutrients with external taste receptor neurons. Drosophila possesses multiple taste organs that are distributed throughout its body. However, the role of different taste organs in feeding remains poorly understood. By blocking subsets of sweet taste receptor neurons, we show that receptor neurons in the legs are required for immediate sugar choice. Furthermore, we identify two anatomically distinct classes of sweet taste receptor neurons in the leg. The axonal projections of one class terminate in the thoracic ganglia, whereas the other projects directly to the brain. These two classes are functionally distinct: the brain-projecting neurons are involved in feeding initiation, whereas the thoracic ganglia-projecting neurons play a role in sugar-dependent suppression of locomotion. Distinct receptor neurons for the same taste quality may coordinate early appetitive responses, taking advantage of the legs as the first appendages to contact food., Locating food sources is essential for the survival of animals. Here, the authors identify two functionally and anatomically distinct classes of sweet taste receptor neurons in Drosophila legs, involved in feeding initiation and sugar-dependent suppression of locomotion.

Odor-shock memory in Drosophila melanogaster consists of heterogeneous components each with different dynamics. We report that a null mutant for the evolutionarily conserved synaptic protein Synapsin entails a memory deficit selectively in early memory, leaving later memory as well as sensory motor function unaffected. Notably, a consolidated memory component remaining after cold-anesthesia is not impaired, suggesting that only anesthesia-sensitive memory [ASM] depends on Synapsin. The lack of Synapsin does not further impair the memory deficit of mutants for the rutabaga gene encoding the type I adenylyl cyclase. This suggests that cAMP signaling, through a Synapsin-dependent mechanism, may underlie the formation of a labile memory component.

Previously, we demonstrated that visual and olfactory associative memories of Drosophila share mushroom body (MB) circuits (Vogt et al., 2014). Unlike for odor representation, the MB circuit for visual information has not been characterized. Here, we show that a small subset of MB Kenyon cells (KCs) selectively responds to visual but not olfactory stimulation. The dendrites of these atypical KCs form a ventral accessory calyx (vAC), distinct from the main calyx that receives olfactory input. We identified two types of visual projection neurons (VPNs) directly connecting the optic lobes and the vAC. Strikingly, these VPNs are differentially required for visual memories of color and brightness. The segregation of visual and olfactory domains in the MB allows independent processing of distinct sensory memories and may be a conserved form of sensory representations among insects.

SummaryMotivation controls behavior [1]. A variety of food-related behaviors undergo motivational modulation by hunger, satiety, and other states [2–4]. Here we searched for critical satiation factors modulating approach to an odor associated with sugar reward in Drosophila melanogaster. We selectively manipulated different parameters associated with feeding, such as internal glucose levels, and determined which are required for suppressing conditioned odor approach. Surprisingly, glucose levels in the hemolymph, nutritional value, sweetness of the food, and ingested volume (above a minimal threshold) did not influence behavior suppression. Instead, we found that the total osmolarity of ingested food is a critical satiation factor. In parallel, we found that conditioned approach is transiently suppressed by artificial stimulation of adipokinetic hormone (AKH) expressing corpora cardiaca cells, which causes elevation of hemolymph carbohydrate and lipid concentrations [5, 6]. This result implies that a rise in hemolymph osmolarity, without the experience of feeding, is sufficient to satiate conditioned odor approach. AKH stimulation did not affect innate sugar preference, suggesting that multiple satiation signals control different sets of appetitive behaviors.