Allatostatin-A neurons inhibit feeding behavior in adult Drosophila
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.
© 2012 by the National Academy of Sciences. Freely available online through the PNAS open access option. Contributed by David J. Anderson, January 17, 2012 (sent for review October 20, 2011). We thank L. Wang and H. Inagaki for helpful comments on the manuscript, G. Carvalho and W. W. Ja for advice on the CAFE assay, B. Al-Anzi and members of the Anderson laboratory for helpful discussions. T.D.T. was supported by a Caltech Biology Divisional Fellowship, a National Institutes of Health Postdoctoral Training Grant (NS007251), and an individual National Research Service Award Fellowship (5F32NS058132). A.C.H. was supported by a Howard Hughes Medical Institute (HHMI) Predoctoral Fellowship and by National Science Foundation Frontiers in Integrative Biological Research Grant EF-0623527 (M. J. Dickinson, principal investigator). D.J.A. is an investigator of the HHMI. Author contributions: A.C.H. and D.J.A. designed research; A.C.H. performed research; A.C.H. and T.D.T. contributed new reagents/analytic tools; A.C.H. and D.J.A. analyzed data; and A.C.H. and D.J.A. wrote the paper. The authors declare no conflict of interest.
Published - Hergarden2012p17510P_Natl_Acad_Sci_Usa.pdf
Supplemental Material - pnas.201200778SI.pdf