Nature Neuroscience
- 9, 1041 - 1049 (2006)
Published online: 16 July 2006; Corrected online: 03 August 2006 | doi:10.1038/nn1740
BK calcium-activated potassium channels regulate circadian behavioral rhythms and pacemaker outputAndrea L Meredith1, 4, Steven W Wiler1, Brooke H Miller2, Joseph S Takahashi2, Anthony A Fodor1, Norman F Ruby3 & Richard W Aldrich11
Department of Molecular and Cellular Physiology and Howard Hughes Medical Institute, Stanford University, Stanford, California 94305, USA. 2
Department of Neurobiology and Physiology and Howard Hughes Medical Institute, Northwestern University, Evanston, Illinois 60208, USA. 3
Department of Biological Sciences, Stanford University, Stanford, California 94305, USA. 4
Present address: Department of Physiology, University of Maryland School of Medicine, 655 West Baltimore Street, Baltimore, Maryland 21201, USA.
Correspondence should be addressed to Andrea L Meredith ameredith@som.umaryland.edu Spontaneous action potentials in the suprachiasmatic nucleus (SCN) are necessary for normal circadian timing of behavior in mammals. The SCN exhibits a daily oscillation in spontaneous firing rate (SFR), but the ionic conductances controlling SFR and the relationship of SFR to subsequent circadian behavioral rhythms are not understood. We show that daily expression of the large conductance Ca2+-activated K+ channel (BK) in the SCN is controlled by the intrinsic circadian clock. BK channel–null mice (Kcnma1
-/-) have increased SFRs in SCN neurons selectively at night and weak circadian amplitudes in multiple behaviors timed by the SCN. Kcnma1-/- mice show normal expression of clock genes such as Arntl (Bmal1), indicating a role for BK channels in SCN pacemaker output, rather than in intrinsic time-keeping. Our findings implicate BK channels as important regulators of the SFR and suggest that the SCN pacemaker governs the expression of circadian behavioral rhythms through SFR modulation.
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