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: A total of 46.27% of mice responded to the CMS procedure by a significant reduction in sucrose preference (P=.001) (Figure 1a), which was paralleled by a significant reduction in the percentage of body weight gain (P=.001) during the experimental period (Figure 1b) and were termed “anhedonic.” Change in sucrose preference and percentage of body weight gain was comparable between the remaining “nonanhedonic” (53.73% of all animals) and handled-only “control” mice. Cosinor analysis of clock gene expression in the BLA of anhedonic mice revealed a disruption in the diurnal expression pattern of all clock genes analyzed (Table 1a). For all clock genes (with the exception of Bmal1, where the induction of a depressive-like state resulted in a shift in the rhythmic expression pattern as indicated by an alteration in the peak time [from ZT16 to ZT23] compared with control mice [Table 1b]), the diurnal rhythmicity in clock gene expression was abolished in anhedonic mice (Table 1a; Figure 2; Supplementary Table S1).
Affiliation: Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Austria.