In a Rat Model of Night Work, Activity during the Normal Resting Phase Produces Desynchrony in the Hypothalamus

Dec 8, 2010Journal of biological rhythms

Nighttime activity in rats causes timing mismatch in the brain's daily rhythm center

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Abstract

Night work in a rat model led to altered diurnal rhythms of c-Fos and induced a rhythm of PER1 in specific hypothalamic regions.

Wakefulness and activity during the normal resting phase shifted daily rhythms in the hypothalamus.
Increased activity of orexin-positive neurons and c-Fos was observed during the working period.
Colocalization of c-Fos in orexin-positive cells did not increase despite heightened activity.
The suprachiasmatic nucleus and paraventricular nucleus remained aligned with the light/dark cycle.
Internal desynchrony was indicated at the level of hypothalamic output projections from the suprachiasmatic nucleus.

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Internal synchrony among external cycles and internal oscillators allows adaptation of physiology to cyclic demands for homeostasis. Night work and shift work lead to a disrupted phase relationship between external time cues and internal rhythms, also losing internal coherence among oscillations. This process results in internal desynchrony (ID) in which behavioral, hormonal, and metabolic variables cycle out of phase. It is still not clear whether ID originates at a peripheral or at a central level. In order to determine the possible role of hypothalamic oscillators in ID, we explored with a rat model of "night work" daily rhythms of activity and clock gene expression in the hypothalamus. This study provides evidence that wakefulness and activity during the normal resting phase lead to a shift in the diurnal rhythms of c-Fos and induce a rhythm of PER1 in the arcuate and dorsomedial nucleus of the hypothalamus, both associated with metabolism and regulation of the sleep/wake cycle. Moreover, the number of orexin (ORX)-positive neurons and c-Fos in the perifornical area increased during the working period, suggesting a relevant switch of activity in this brain region induced by the scheduled activity; however, the colocalization of c-Fos in ORX-positive cells was not increased. In contrast, the suprachiasmatic nucleus and the paraventricular nucleus remained locked to the light/dark cycle, resulting in ID in the hypothalamus. Present data suggest that ID occurs already at the level of the first output projections from the SCN, relaying nuclei that transmit temporal signals to other brain areas and to the periphery.

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In a Rat Model of Night Work, Activity during the Normal Resting Phase Produces Desynchrony in the Hypothalamus

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