Literature DB >> 19619568

Accelerated re-entrainment to advanced light cycles in BALB/cJ mice.

Tara A Legates1, Danielle Dunn, E Todd Weber.   

Abstract

Circadian rhythms in mammals are coordinated by the suprachiasmatic nuclei (SCN) of the hypothalamus, which are most potently synchronized to environmental light-dark cycles. Large advances in the light-dark cycle typically yield gradual advances in activity rhythms on the order of 1-2h per day until re-entrainment is complete due to limitations on the circadian system which are not yet understood. In humans, this delay until re-entrainment is accomplished is experienced as jetlag, with accompanying symptoms of malaise, decreased cognitive performance, sleep problems and gastrointestinal distress. In these experiments, locomotor rhythms of BALB/cJ mice monitored by running wheels were shown to re-entrain to large 6- or 8-hour shifts of the light-dark cycle within 1-2 days, as opposed to the 5-7 days required for C57BL/6J mice. A single-day 6-hour advance of the LD cycle followed by release to constant darkness yielded similar phase shifts, demonstrating that exaggerated re-entrainment is not explained by masking of activity by the light-dark cycle. Responses in BALB/cJ mice were similar when monitored instead by motion detectors, indicating that wheel-running exercise does not influence the magnitude of responses. Neither brief (15 min) light exposure late during subjective nighttime nor 6-hour delays of the light-dark cycle produced exaggerated locomotor phase shifts, indicating that BALB/cJ mice do not merely experience enhanced sensitivity to light. Fos protein was expressed in cells of the SCN following acute light exposure at ZT10 of their previous light-dark cycle, a normally non-responsive time in the circadian cycle, but only in BALB/cJ (and not C57BL/6J) mice that had been subjected two days earlier to a single-day 6-hour advance of the light-dark cycle, indicating that their SCN had been advanced by that treatment. BALB/cJ mice may thus serve as a useful comparative model for studying molecular and physiological processes that limit responsiveness of circadian clocks to photic input.

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Year:  2009        PMID: 19619568      PMCID: PMC2746879          DOI: 10.1016/j.physbeh.2009.07.007

Source DB:  PubMed          Journal:  Physiol Behav        ISSN: 0031-9384


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  5 in total

1.  Epigenomics: maternal high-fat diet exposure in utero disrupts peripheral circadian gene expression in nonhuman primates.

Authors:  Melissa Suter; Philip Bocock; Lori Showalter; Min Hu; Cynthia Shope; Robert McKnight; Kevin Grove; Robert Lane; Kjersti Aagaard-Tillery
Journal:  FASEB J       Date:  2010-11-19       Impact factor: 5.191

2.  Measuring circadian and acute light responses in mice using wheel running activity.

Authors:  Tara A LeGates; Cara M Altimus
Journal:  J Vis Exp       Date:  2011-02-04       Impact factor: 1.355

3.  Rapid Response and Slow Recovery of the H3K4me3 Epigenomic Marker in the Liver after Light-mediated Phase Advances of the Circadian Clock.

Authors:  Dmytro Grygoryev; Michael R Rountree; Furaha Rwatambuga; Anna Ohlrich; Ayaka Kukino; Matthew P Butler; Charles N Allen; Mitchell S Turker
Journal:  J Biol Rhythms       Date:  2018-06-11       Impact factor: 3.649

Review 4.  Evidence for Internal Desynchrony Caused by Circadian Clock Resetting.

Authors:  Shannon K Nicholls; Leandro P Casiraghi; Wanqi Wang; E Todd Weber; Mary E Harrington
Journal:  Yale J Biol Med       Date:  2019-06-27

5.  A novel mouse model for vulnerability to alcohol dependence induced by early-life adversity.

Authors:  Agbonlahor Okhuarobo; Jessica L Bolton; Ighodaro Igbe; Eric P Zorrilla; Tallie Z Baram; Candice Contet
Journal:  Neurobiol Stress       Date:  2020-11-30
  5 in total

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