title: Accelerated re-entrainment to advanced light cycles in BALB/cJ mice.
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.
authors.affiliation: Rider University, Lawrenceville, NJ 08648, USA.
authors.forename: Tara A
authors.initials: TA
authors.lastname: Legates
authors.forename: Danielle
authors.initials: D
authors.lastname: Dunn
authors.forename: E Todd
authors.initials: ET
authors.lastname: Weber
mesh_terms: D000054:Acceleration; D000704:Analysis of Variance; D000818:Animals; D001522:Behavior, Animal; D002940:Circadian Rhythm / Q000502:physiology; D005260:Female; D005786:Gene Expression Regulation / Q000502:physiology; D008027:Light; D008124:Locomotion / Q000502:physiology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D010775:Photic Stimulation; D017440:Photoperiod; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D013045:Species Specificity; D013493:Suprachiasmatic Nucleus / Q000378:metabolism; D013997:Time Factors
chemical_list: D016760:Proto-Oncogene Proteins c-fos