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      Electrical hyperexcitation of lateral ventral pacemaker neurons desynchronizes downstream circadian oscillators in the fly circadian circuit and induces multiple behavioral periods.

      The Journal of neuroscience : the official journal of the Society for Neuroscience
      Amino Acid Sequence, Animals, Animals, Genetically Modified, Bacterial Proteins, genetics, physiology, Behavior, Animal, Biological Clocks, Brain, cytology, Circadian Rhythm, Drosophila Proteins, Drosophila melanogaster, Membrane Potentials, Molecular Sequence Data, Motor Activity, Neurons, Neuropeptides, Oocytes, Point Mutation, Potassium Channels, Recombinant Fusion Proteins, Single-Blind Method, Sodium Channels, Xenopus laevis

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          Abstract

          Coupling of autonomous cellular oscillators is an essential aspect of circadian clock function but little is known about its circuit requirements. Functional ablation of the pigment-dispersing factor-expressing lateral ventral subset (LNV) of Drosophila clock neurons abolishes circadian rhythms of locomotor activity. The hypothesis that LNVs synchronize oscillations in downstream clock neurons was tested by rendering the LNVs hyperexcitable via transgenic expression of a low activation threshold voltage-gated sodium channel. When the LNVs are made hyperexcitable, free-running behavioral rhythms decompose into multiple independent superimposed oscillations and the clock protein oscillations in the dorsal neuron 1 and 2 subgroups of clock neurons are phase-shifted. Thus, regulated electrical activity of the LNVs synchronize multiple oscillators in the fly circadian pacemaker circuit.

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