The European journal of neuroscienceOct 1, 2018

Repeated disruptions to daily rhythms change how the body’s internal clock resets

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Mar 28, 2026

Abstract

Exposure to a 20-hour light cycle for over a month significantly alters circadian rhythms in male mice.

A single phase advance in the light:dark cycle can disrupt neural circadian rhythms within the suprachiasmatic nucleus (SCN).
Chronic exposure to disruptive light conditions affects the synchronization between SCN and peripheral tissues.
Dissection timing strongly influences the circadian phase of PER2::LUC bioluminescent rhythms, varying by tissue type.
White adipose tissue exhibits significant resetting by dissection, while thymus phase shows independence from dissection timing.
Prior light exposure leads to strong resetting of SCN phase in mice subjected to a 20-hour light cycle.

Simplified

A single phase advance of the light:dark (LD) cycle can temporarily disrupt synchrony of neural circadian rhythms within the suprachiasmatic nucleus (SCN) and between the SCN and peripheral tissues. Compounding this, modern life can involve repeated disruptive light conditions. To model chronic disruption to the circadian system, we exposed male mice to more than a month of a 20-hr light cycle (LD10:10), which mice typically cannot entrain to. Control animals were housed under LD12:12. We measured locomotor activity and body temperature rhythms in vivo, and rhythms of PER2::LUC bioluminescence in SCN and peripheral tissues ex vivo. Unexpectedly, we discovered strong effects of the time of dissection on circadian phase of PER2::LUC bioluminescent rhythms, which varied across tissues. White adipose tissue was strongly reset by dissection, while thymus phase appeared independent of dissection timing. Prior light exposure impacted the SCN, resulting in strong resetting of SCN phase by dissection for mice housed under LD10:10, and weak phase shifts by time of dissection in SCN from control LD12:12 mice. These findings suggest that exposure to circadian disruption may desynchronize SCN neurons, increasing network sensitivity to perturbations. We propose that tissues with a weakened circadian network, such as the SCN under disruptive light conditions, or with little to no coupling, for example, some peripheral tissues, will show increased resetting effects. In particular, exposure to light at inconsistent circadian times on a recurring weekly basis disrupts circadian rhythms and alters sensitivity of the SCN neural pacemaker to dissection time.

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Repeated disruptions to daily rhythms change how the body’s internal clock resets

Abstract

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