@article {47039, title = {A subset of serotonergic neurons evokes hunger in adult Drosophila.}, journal = {Current Biology : CB}, volume = {25}, year = {2015}, month = {2015 Sep 2}, pages = {2435-40}, abstract = {

Hunger is a complex motivational state that drives multiple behaviors. The sensation of hunger is caused by an imbalance between energy intake and expenditure. One immediate response to hunger is increased food consumption. Hunger also modulates behaviors related to food seeking such as increased locomotion and enhanced sensory sensitivity in both insects [1-5] and vertebrates [6, 7]. In addition, hunger can promote the expression of food-associated memory [8, 9]. Although progress is being made [10], how hunger is represented in the brain and how it coordinates these behavioral responses is not fully understood in any system. Here, we use Drosophila melanogaster to identify neurons encoding hunger. We found a small group of neurons that, when activated, induced a fed fly to eat as though it were starved, suggesting that these neurons are downstream of the metabolic regulation of hunger. Artificially activating these neurons also promotes appetitive memory performance in sated flies, indicating that these neurons are not simply feeding command neurons but likely play a more general role in encoding hunger. We determined that the neurons relevant for the feeding effect are serotonergic and project broadly within the brain, suggesting a possible mechanism for how various responses to hunger are coordinated. These findings extend our\ understanding of the neural circuitry that drives feeding and enable future exploration of how state influences neural activity within this circuit.

}, issn = {1879-0445}, doi = {10.1016/j.cub.2015.08.005}, author = {Albin, Stephanie D and Kaun, Karla R and Knapp, Jon-Michael and Chung, Phuong and Heberlein, Ulrike and Simpson, Julie H} } @article {46427, title = {NF-κB, IκB, and IRAK control glutamate receptor density at the Drosophila NMJ.}, journal = {Neuron}, volume = {55}, year = {2007}, month = {2007 Sep 20}, pages = {859-73}, abstract = {

NF-κB signaling has been implicated in neurodegenerative disease, epilepsy, and neuronal plasticity. However, the cellular and molecular activity of NF-κB signaling within the nervous system remains to be clearly defined. Here,\ we show that the NF-κB and IκB homologs Dorsal and Cactus surround postsynaptic glutamate receptor (GluR) clusters at the Drosophila\ NMJ. We then show that mutations in dorsal, cactus, and IRAK/pelle kinase specifically impair GluR levels, assayed immunohistochemically and electrophysiologically, without affecting NMJ growth, the size of the postsynaptic density, or homeostatic plasticity. Additional genetic experiments support the conclusion that cactus functions in concert with, rather than in opposition to, dorsal and pelle in this process. Finally, we provide evidence that Dorsal and Cactus act\ posttranscriptionally, outside the nucleus, to control GluR density. Based upon our data we speculate that Dorsal, Cactus, and Pelle could function together, locally at the postsynaptic density, to specify GluR levels.

}, keywords = {Developmental Biology, molecular neurology, signaling}, doi = {10.1016/j.neuron.2007.08.005}, author = {Heckscher, Elizabeth S and Fetter, Richard D and Marek, Kurt W and Albin, Stephanie D and Davis, Graeme W} }