Allatostatin-A neurons inhibit feeding behavior in adult Drosophila

Abstract

How the brain translates changes in internal metabolic state or perceived food quality into alterations in feeding behavior remains poorly understood. Studies in Drosophila larvae have yielded information about neuropeptides and circuits that promote feeding, but a peptidergic neuron subset whose activation inhibits feeding in adult flies, without promoting metabolic changes that mimic the state of satiety, has not been identified. Using genetically based manipulations of neuronal activity, we show that activation of neurons (or neuroendocrine cells) expressing the neuropeptide allatostatin A (AstA) inhibits or limits several starvation-induced changes in feeding behavior in adult Drosophila, including increased food intake and enhanced behavioral responsiveness to sugar. Importantly, these effects on feeding behavior are observed in the absence of any measurable effects on metabolism or energy reserves, suggesting that AstA neuron activation is likely a consequence, not a cause, of metabolic changes that induce the state of satiety. These data suggest that activation of AstA-expressing neurons promotes food aversion and/or exerts an inhibitory influence on the motivation to feed and implicate these neurons and their associated circuitry in the mechanisms that translate the state of satiety into alterations in feeding behavior.homeostasis | satiation | foraging | proboscis extension reflex | neuromodulation T o maintain energy homeostasis, the brain translates changes in internal metabolic state into alterations in feeding behavior. Understanding how this translation occurs at the molecular and neural circuit levels is of fundamental importance both as a general model for state-dependent modification of behavior and also for its relevance to human obesity and associated diabetic and cardiovascular disease (1). Drosophila melanogaster provides an excellent model system to study feeding behavior (2, 3) due to its powerful genetics, and because many elements of metabolic homeostasis are conserved between flies and mammals (2, 4-6).

Peptidomics of Neuropeptidergic Tissues of the Tsetse FlyGlossina morsitans morsitans

“…The PM contained two of the predicted neuropeptides. The presence of AstA peptides in the CNS and midgut has previously been reported in other dipterans including D. melanogaster [33,[35][36][37], the cabbage root fly Delia radicum larvae, the midge Chironomus riparius, and mosquitoes Aedes aegypti and Anopheles albimanus [36,[38][39][40][41].…”

Modification of feeding circuits in the evolution of social behavior

“…In Drosophila, hugin is involved in the decision-making process of whether to eat a novel food source (Melcher and Pankratz, 2005), while in rodents, Neuromedin U suppresses food intake (Howard et al, 2000). There are also some invertebrate-specific neuropeptides that regulate feeding behavior, including allatostatins (Hergarden et al, 2012) and sulfakinins (Wei et al, 2000), which both suppress feeding behavior in insects. Finally, a recent study in Drosophila suggests some neurons in the ellipsoid body of the brain central complex stimulate feeding behavior, and are thus functionally similar to the vertebrate AgRP/NPY neurons (Park et al, 2016).…”

Integration of Taste and Calorie Sensing inDrosophila

“…Preference for caloric sugars is potentiated by starvation Starvation is known to enhance feeding behaviors and taste sensitivity in flies (Barton Browne, 1975;Scheiner et al, 2004;Farhadian et al, 2012;Hergarden et al, 2012;Inagaki et al, 2012). To test the effects of starvation on preference for caloric sugars, we fooddeprived flies for 8 or 24 h and measured their preference for the mixture of 20% sucrose and 80% mannose versus L-fucose.…”