Visualizing jet lag in the mouse suprachiasmatic nucleus and peripheral circadian timing system

Nov 27, 2008The European journal of neuroscience

Tracking jet lag effects in the mouse brain's internal clock and body timing system

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Abstract

Significant differences in the resynchronization kinetics of circadian rhythms in mice were observed after a 6-hour phase advance of the light cycle.

The phase distribution of Period2-expressing neurons in the suprachiasmatic nuclei (SCN) widened the day after the light cycle shift.
Cells in the ventral SCN initially shifted more than those in the dorsal SCN, but no strict division between these regions was found.
A population of fast-shifting cells in the SCN exhibited a ventral-dorsal gradient in their anatomical distribution.
Full resynchronization of the SCN and peripheral organs was not achieved until after 8 days in the new light cycle.

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Circadian rhythms regulate most physiological processes. Adjustments to circadian time, called phase shifts, are necessary following international travel and on a more frequent basis for individuals who work non-traditional schedules such as rotating shifts. As the disruption that results from frequent phase shifts is deleterious to both animals and humans, we sought to better understand the kinetics of resynchronization of the mouse circadian system to one of the most disruptive phase shifts, a 6-h phase advance. Mice bearing a luciferase reporter gene for mPer2 were subjected to a 6-h advance of the light cycle and molecular rhythms in suprachiasmatic nuclei (SCN), thymus, spleen, lung and esophagus were measured periodically for 2 weeks following the shift. For the SCN, the master pacemaker in the brain, we employed high-resolution imaging of the brain slice to describe the resynchronization of rhythms in single SCN neurons during adjustment to the new light cycle. We observed significant differences in shifting kinetics among mice, among organs such as the spleen and lung, and importantly among neurons in the SCN. The phase distribution among all Period2-expressing SCN neurons widened on the day following a shift of the light cycle, which was partially due to cells in the ventral SCN exhibiting a larger initial phase shift than cells in the dorsal SCN. There was no clear delineation of ventral and dorsal regions, however, as the SCN appear to have a population of fast-shifting cells whose anatomical distribution is organized in a ventral-dorsal gradient. Full resynchronization of the SCN and peripheral timing system, as measured by a circadian reporter gene, did not occur until after 8 days in the advanced light cycle.

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Visualizing jet lag in the mouse suprachiasmatic nucleus and peripheral circadian timing system

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