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      Even-skipped + interneurons are core components of a sensorimotor circuit that maintains left-right symmetric muscle contraction amplitude

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          Summary

          Bilaterally symmetric motor patterns—those in which left-right pairs of muscles contract synchronously and with equal amplitude (such as breathing, smiling, whisking, locomotion)—are widespread throughout the animal kingdom. Yet surprisingly little is known about the underlying neural circuits. We performed a thermogenetic screen to identify neurons required for bilaterally symmetric locomotion in Drosophila larvae, and identified the evolutionarily-conserved Even-skipped + interneurons (Eve/Evx). Activation or ablation of Eve + interneurons disrupted bilaterally symmetric muscle contraction amplitude, without affecting the timing of motor output. Eve + interneurons are not rhythmically active, and thus function independently of the locomotor CPG. GCaMP6 calcium imaging of Eve + interneurons in freely-moving larvae showed left-right asymmetric activation that correlated with larval behavior. TEM reconstruction of Eve + interneuron inputs and outputs showed that the Eve + interneurons are at the core of a sensorimotor circuit capable of detecting and modifying body wall muscle contraction.

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          Author and article information

          Journal
          8809320
          1600
          Neuron
          Neuron
          Neuron
          0896-6273
          1097-4199
          20 October 2015
          01 October 2015
          21 October 2015
          21 October 2016
          : 88
          : 2
          : 314-329
          Affiliations
          [1 ]Institute of Neuroscience, University of Oregon, Eugene, OR 97403
          [2 ]Institute of Molecular Biology, University of Oregon, Eugene, OR 97403
          [3 ]Howard Hughes Medical Institute, University of Oregon, Eugene, OR 97403
          [4 ]Janelia Farms Research Campus, HHMI, Ashburn, VA 20147
          [5 ]Department of Zoology, University of Cambridge, Cambridge CB2 3EJ
          Author notes
          [6]

          Present address: Department of Molecular Genetics and Cell Biology, University of Chicago, Chicago, IL, 60637

          Article
          PMC4619170 PMC4619170 4619170 nihpa728946
          10.1016/j.neuron.2015.09.009
          4619170
          26439528
          1d8ae945-4195-47b6-9599-fefc576e4d29
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