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Cell. 2015 Aug 13;162(4):836-48. doi: 10.1016/j.cell.2015.07.036.

A Conserved Bicycle Model for Circadian Clock Control of Membrane Excitability.

Author information

1
Department of Neurobiology, Northwestern University, Evanston, IL 60208, USA.
2
Medical Scientist Training Program, James Franck Institute, Department of Chemistry, Institute for Biophysical Dynamics, University of Chicago, Chicago, IL 60637, USA.
3
Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA.
4
Department of Biology, University of Iowa, Iowa City, IA 52242, USA.
5
Institute for Genomics and Systems Biology, University of Chicago, Chicago, IL 60637, USA.
6
Department of Mathematical Sciences, New Jersey Institute of Technology, Newark, NJ 07102, USA.
7
Department of Neurobiology, Northwestern University, Evanston, IL 60208, USA. Electronic address: r-allada@northwestern.edu.

Abstract

Circadian clocks regulate membrane excitability in master pacemaker neurons to control daily rhythms of sleep and wake. Here, we find that two distinctly timed electrical drives collaborate to impose rhythmicity on Drosophila clock neurons. In the morning, a voltage-independent sodium conductance via the NA/NALCN ion channel depolarizes these neurons. This current is driven by the rhythmic expression of NCA localization factor-1, linking the molecular clock to ion channel function. In the evening, basal potassium currents peak to silence clock neurons. Remarkably, daily antiphase cycles of sodium and potassium currents also drive mouse clock neuron rhythms. Thus, we reveal an evolutionarily ancient strategy for the neural mechanisms that govern daily sleep and wake.

PMID:
26276633
PMCID:
PMC4537776
DOI:
10.1016/j.cell.2015.07.036
[Indexed for MEDLINE]
Free PMC Article

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