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      Postprandial sleep mechanics in Drosophila

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          Abstract

          Food consumption is thought to induce sleepiness. However, little is known about how postprandial sleep is regulated. Here, we simultaneously measured sleep and food intake of individual flies and found a transient rise in sleep following meals. Depending on the amount consumed, the effect ranged from slightly arousing to strongly sleep inducing. Postprandial sleep was positively correlated with ingested volume, protein, and salt—but not sucrose—revealing meal property-specific regulation. Silencing of leucokinin receptor (Lkr) neurons specifically reduced sleep induced by protein consumption. Thermogenetic stimulation of leucokinin (Lk) neurons decreased whereas Lk downregulation by RNAi increased postprandial sleep, suggestive of an inhibitory connection in the Lk-Lkr circuit. We further identified a subset of non-leucokininergic cells proximal to Lkr neurons that rhythmically increased postprandial sleep when silenced, suggesting that these cells are cyclically gated inhibitory inputs to Lkr neurons. Together, these findings reveal the dynamic nature of postprandial sleep.

          DOI: http://dx.doi.org/10.7554/eLife.19334.001

          eLife digest

          Many of us have experienced feelings of sleepiness after a large meal. However, there is little scientific evidence that this “food coma” effect is real. If it is, it may vary between individuals, or depend on the type of food consumed. This variability makes it difficult to study the causes of post-meal sleepiness.

          Murphy et al. have now developed a system that can measure fruit fly sleep and feeding behavior at the same time. Recordings using this system reveal that after a meal, flies sleep more for a short period before returning to a normal state of wakefulness. The sleep period lasts around 20-40 minutes, with flies that ate more generally sleeping more.

          Further investigation revealed that salty or protein-rich foods promote sleep, whereas sugary foods do not. By using genetic tools to turn on and off neurons in the fly brain, Murphy et al. identified a number of brain circuits that play a role in controlling post-meal sleepiness. Some of these respond specifically to the consumption of protein. Others are sensitive to the fruit fly’s internal clock, reducing post-meal sleepiness only around dusk. Thus, post-meal sleepiness can be regulated in a number of different ways.

          Future experiments are now needed to explore the genes and circuits that enable meal size and the protein or salt content of food to drive sleep. In nature, sleep is likely a vulnerable state for animals. Thus, another challenge will be to uncover why post-meal sleep is important. Does sleeping after a meal boost digestion? Or might it help animals to form memories about a food source, making it easier to find similar food in the future?

          DOI: http://dx.doi.org/10.7554/eLife.19334.002

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          Most cited references41

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          NIH Image to ImageJ: 25 years of image analysis.

          For the past 25 years NIH Image and ImageJ software have been pioneers as open tools for the analysis of scientific images. We discuss the origins, challenges and solutions of these two programs, and how their history can serve to advise and inform other software projects.
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            Motor control in a Drosophila taste circuit.

            Tastes elicit innate behaviors critical for directing animals to ingest nutritious substances and reject toxic compounds, but the neural basis of these behaviors is not understood. Here, we use a neural silencing screen to identify neurons required for a simple Drosophila taste behavior and characterize a neural population that controls a specific subprogram of this behavior. By silencing and activating subsets of the defined cell population, we identify the neurons involved in the taste behavior as a pair of motor neurons located in the subesophageal ganglion (SOG). The motor neurons are activated by sugar stimulation of gustatory neurons and inhibited by bitter compounds; however, experiments utilizing split-GFP detect no direct connections between the motor neurons and primary sensory neurons, indicating that further study will be necessary to elucidate the circuitry bridging these populations. Combined, these results provide a general strategy and a valuable starting point for future taste circuit analysis.
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              Altered electrical properties in Drosophila neurons developing without synaptic transmission.

              We examine the role of synaptic activity in the development of identified Drosophila embryonic motorneurons. Synaptic activity was blocked by both pan-neuronal expression of tetanus toxin light chain (TeTxLC) and by reduction of acetylcholine (ACh) using a temperature-sensitive allele of choline acetyltransferase (Cha(ts2)). In the absence of synaptic activity, aCC and RP2 motorneurons develop with an apparently normal morphology and retain their capacity to form synapses. However, blockade of synaptic transmission results in significant changes in the electrical phenotype of these neurons. Specifically, increases are seen in both voltage-gated inward Na(+) and voltage-gated outward K(+) currents. Voltage-gated Ca(2+) currents do not change. The changes in conductances appear to promote neuron excitability. In the absence of synaptic activity, the number of action potentials fired by a depolarizing ramp (-60 to +60 mV) is increased and, in addition, the amplitude of the initial action potential fired is also significantly larger. Silencing synaptic input to just aCC, without affecting inputs to other neurons, demonstrates that the capability to respond to changing levels of synaptic excitation is intrinsic to these neurons. The alteration to electrical properties are not permanent, being reversed by restoration of normal synaptic function. Whereas our data suggest that synaptic activity makes little or no contribution to the initial formation of embryonic neural circuits, the electrical development of neurons that constitute these circuits seems to depend on a process that requires synaptic activity.
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                Author and article information

                Contributors
                Role: Reviewing editor
                Journal
                eLife
                Elife
                eLife
                eLife
                eLife
                eLife Sciences Publications, Ltd
                2050-084X
                22 November 2016
                2016
                : 5
                : e19334
                Affiliations
                [1 ]deptDepartment of Metabolism and Aging , The Scripps Research Institute , Jupiter, United States
                [2 ]deptProgram in Integrative Biology and Neuroscience , Florida Atlantic University , Jupiter, United States
                [3 ]deptDepartment of Neuroscience , The Scripps Research Institute , Jupiter, United States
                [4 ]deptRadcliffe Institute for Advanced Study , Harvard University , Cambridge, United States
                [5 ]deptJP Scott Center for Neuroscience, Mind and Behavior , Bowling Green State University , Bowling Green, United States
                [6]University of California, Berkeley , United States
                [7]University of California, Berkeley , United States
                Author notes
                Author information
                http://orcid.org/0000-0002-4003-7356
                Article
                19334
                10.7554/eLife.19334
                5119887
                27873574
                2e6ee981-28d1-46ad-9687-0c9c962f4d98
                © 2016, Murphy et al

                This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.

                History
                : 03 July 2016
                : 27 October 2016
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;
                Award ID: R21DK092735
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100000863, Ellison Medical Foundation;
                Award ID: New Scholar in Aging award
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100001642, Glenn Foundation for Medical Research;
                Award ID: Medical Research Award for Research in Biological Mechanisms of Aging
                Award Recipient :
                The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
                Categories
                Neuroscience
                Research Article
                Custom metadata
                2.5
                Evidence of food coma has been found in fruit flies, allowing the properties that drive postprandial sleep and their underlying genetic and neuronal mechanisms to be described.

                Life sciences
                feeding,sleep,behavior,neurogenetics,nutrition,d. melanogaster
                Life sciences
                feeding, sleep, behavior, neurogenetics, nutrition, d. melanogaster

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