Journal
JOURNAL OF NEUROSCIENCE
Volume 25, Issue 33, Pages 7682-7686Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2211-05.2005
Keywords
circadian rhythm; calcium; potassium; suprachiasmatic nucleus; Period 1; PERIOD 2
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Funding
- NHLBI NIH HHS [HL71510, R01 HL071510] Funding Source: Medline
- NIMH NIH HHS [R01 MH062517, MH62517, R01 MH062517-03] Funding Source: Medline
- NINDS NIH HHS [R01 NS055361-05] Funding Source: Medline
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Generation of mammalian circadian rhythms involves molecular transcriptional and translational feedback loops. It is not clear how membrane events interact with the intracellular molecular clock or whether membrane activities are involved in the actual generation of the circadian rhythm. We examined the role of membrane potential and calcium (Ca2+) influx in the expression of the circadian rhythm of the clock gene Period 1 (Per1) within the rat suprachiasmatic nucleus (SCN), the master pacemaker controlling circadian rhythmicity. Membrane hyperpolarization, caused by lowering the extracellular concentration of potassium or blocking Ca2+ influx in SCN cultures by lowering [Ca2+], reversibly abolished the rhythmic expression of Per1. In addition, the amplitude of Per1 expression was markedly decreased by voltage-gated Ca2+ channel antagonists. A similar result was observed for mouse Per1 and PER2. Together, these results strongly suggest that a transmembrane Ca2+ flux is necessary for sustained molecular rhythmicity in the SCN. We propose that periodic Ca2+ influx, resulting from circadian variations in membrane potential, is a critical process for circadian pacemaker function.
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