Diurnal oscillation of amygdala clock gene expression and loss of synchrony in a mouse model of depression.
Bottom Line: Disturbances in circadian rhythm-related physiological and behavioral processes are frequently observed in depressed patients and several clock genes have been identified as risk factors for the development of mood disorders.Clock gene desynchronization was accompanied by disruption of the diurnal expressional pattern of vascular endothelial growth factor A expression in the basolateral amygdala of anhedonic mice, also reflected in alterations of circulating vascular endothelial growth factor A levels.We propose that aberrant control of diurnal rhythmicity related to depression may indeed directly result from the illness itself and establish an animal model for the further exploration of the molecular mechanisms mediating the involvement of the circadian system in the pathophysiology of mood disorders.
Affiliation: Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Austria.Show MeSH
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Mentions: To exemplarily demonstrate that the observed changes of clock gene expression in anhedonic mice were paralleled by respective alterations of protein levels, BLA protein expression of CLOCK was compared between anhedonic and control mice at ZT12 (Figure 3a). ZT12 was chosen as representative time point, since 2-way ANOVA analysis followed by Bonferroni posthoc tests of mRNA expression levels had indicated significant differences between control and anhedonic mice specifically during the night phase, at ZT12 (P=.2E-4); ZT16 (P=.001); ZT20 (P=1.56E-07), with higher Clock expression in the BLA of anhedonic mice (significant main effect of treatment (F(1,61)=50.72, P=1.43E-09), significant main effect of time points (F(5,61)=4.61, P=.001) and significant interaction between treatment and time points [F(5,61) = 3.60, P=.006]).
Affiliation: Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Austria.