Phase-delay in the light–dark cycle impairs clock gene expression and levels of serotonin, norepinephrine, and their metabolites in the mouse hippocampus and amygdala

Oct 27, 2015Sleep medicine

Delaying the daily light-dark schedule reduces clock gene activity and key brain chemicals in mouse memory and emotion areas

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Abstract

Mice subjected to an 8-hour phase delay in the light-dark cycle showed a longer locomotor activity period of over 24 hours.

Behavioral changes indicated a free-running phenotype with misalignment between light-dark and active-inactive cycles.
Circadian fluctuations of the clock gene Bmal1 were reduced in the amygdala and hippocampus of light-dark-shifted mice.
The expression profiles of the NE/5HT uptake transporter gene Net differed between the Shift and Control groups.
Norepinephrine (NE) and serotonin (5HT) levels in the amygdala increased during the active period in the Shift group.

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OBJECTIVE: A number of animal studies have implicated circadian clock genes in the regulation of mood, anxiety, and reward. However, the effect of misalignment of the environmental light-dark and internal circadian clock on the monoamine system is not fully understood. In the present study, we examined whether an abnormal light-dark schedule would affect behavior-, circadian clock-, and monoamine-related gene expressions, along with monoamine contents in the amygdala and hippocampus of mice.

METHODS: Mice were subjected to an 8-hour phase delay in the light-dark cycle (Shift) every two days for four weeks, and locomotor activity was continuously measured. We examined the circadian expression of clock genes (Per1, Per2, and Bmal1) and genes of the NE/5HT uptake transporters (Net and Sert). In addition, the levels of NE/5HT and their metabolites MHPG/5HIAA were analyzed in the amygdala and hippocampus.

RESULTS: Locomotor activity showed a free-running phenotype with a longer period (>24 hours) and showed misalignment between the light-dark and inactive-active cycles. The amplitude of the day-night fluctuation of Bmal1 expression was reduced in the amygdala and hippocampus of light-dark-shifted mice. Net gene expression in the Shift group showed different profiles compared with the Control group. In addition, NE and 5HT levels in the amygdala of the Shift group increased during the active period.

CONCLUSIONS: The present results suggest that misalignment of the internal and external clocks by continuous shifting of the light-dark cycle affects the circadian clocks and monoamine metabolism in the amygdala and hippocampus of mice.

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Phase-delay in the light–dark cycle impairs clock gene expression and levels of serotonin, norepinephrine, and their metabolites in the mouse hippocampus and amygdala

Abstract

Full Text

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