title: Diurnal oscillation of amygdala clock gene expression and loss of synchrony in a mouse model of depression.
abstract: BACKGROUND
  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. However, the particular involvement of the circadian system in the pathophysiology of depression and its molecular regulatory interface is incompletely understood.
  
  
  METHODS
  A naturalistic animal model of depression based upon exposure to chronic mild stress was used to induce anhedonic behavior in mice. Micro-punch dissection was used to isolate basolateral amygdala tissue from anhedonic mice followed by quantitative real-time PCR-based analysis of gene expression.
  
  
  RESULTS
  Here we demonstrate that chronic mild stress-induced anhedonic behavior is associated with disturbed diurnal oscillation of the expression of Clock, Cry2, Per1, Per3, Id2, Rev-erbα, Ror-β and Ror-γ in the mouse basolateral amygdala. 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Austria.
authors.forename: Giorgia
authors.initials: G
authors.lastname: Savalli
authors.affiliation: Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Austria.
authors.forename: Weifei
authors.initials: W
authors.lastname: Diao
authors.affiliation: Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Austria.
authors.forename: Stefan
authors.initials: S
authors.lastname: Schulz
authors.affiliation: Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Austria.
authors.forename: Kristina
authors.initials: K
authors.lastname: Todtova
authors.affiliation: Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Austria. daniela.pollak@meduniwien.ac.at.
authors.forename: Daniela D
authors.initials: DD
authors.lastname: Pollak
mesh_terms: D000679:Amygdala / Q000378:metabolism*; D059445:Anhedonia; D000818:Animals; D001522:Behavior, Animal; D056926:CLOCK Proteins / Q000235:genetics*; D002940:Circadian Rhythm; D003863:Depression / Q000235:genetics / Q000523:psychology*; D015870:Gene Expression; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D060888:Real-Time Polymerase Chain Reaction; D013315:Stress, Psychological / Q000150:complications*
chemical_list: D056926:CLOCK Proteins
keywords: VEGF; amygdala; chronic mild stress; clock gene; depression