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Anhedonic behavior in cryptochrome 2-deficient mice is paralleled by altered diurnal patterns of amygdala gene expression.
Amino Acids 2015; 47(7):1367-77AA

Abstract

Mood disorders are frequently paralleled by disturbances in circadian rhythm-related physiological and behavioral states and genetic variants of clock genes have been associated with depression. Cryptochrome 2 (Cry2) is one of the core components of the molecular circadian machinery which has been linked to depression, both, in patients suffering from the disease and animal models of the disorder. Despite this circumstantial evidence, a direct causal relationship between Cry2 expression and depression has not been established. Here, a genetic mouse model of Cry2 deficiency (Cry2 (-/-) mice) was employed to test the direct relevance of Cry2 for depression-like behavior. Augmented anhedonic behavior in the sucrose preference test, without alterations in behavioral despair, was observed in Cry2 (-/-) mice. The novelty suppressed feeding paradigm revealed reduced hyponeophagia in Cry2 (-/-) mice compared to wild-type littermates. Given the importance of the amygdala in the regulation of emotion and their relevance for the pathophysiology of depression, potential alterations in diurnal patterns of basolateral amygdala gene expression in Cry2 (-/-) mice were investigated focusing on core clock genes and neurotrophic factor systems implicated in the pathophysiology of depression. Differential expression of the clock gene Bhlhe40 and the neurotrophic factor Vegfb were found in the beginning of the active (dark) phase in Cry2 (-/-) compared to wild-type animals. Furthermore, amygdala tissue of Cry2 (-/-) mice contained lower levels of Bdnf-III. Collectively, these results indicate that Cry2 exerts a critical role in the control of depression-related emotional states and modulates the chronobiological gene expression profile in the mouse amygdala.

Authors+Show Affiliations

Department of Neurophysiology and Neuropharmacology, Center for Physiology and Pharmacology, Medical University of Vienna, Schwarzspanierstrasse, 17, 1090, Vienna, Austria.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25820768

Citation

Savalli, Giorgia, et al. "Anhedonic Behavior in Cryptochrome 2-deficient Mice Is Paralleled By Altered Diurnal Patterns of Amygdala Gene Expression." Amino Acids, vol. 47, no. 7, 2015, pp. 1367-77.
Savalli G, Diao W, Berger S, et al. Anhedonic behavior in cryptochrome 2-deficient mice is paralleled by altered diurnal patterns of amygdala gene expression. Amino Acids. 2015;47(7):1367-77.
Savalli, G., Diao, W., Berger, S., Ronovsky, M., Partonen, T., & Pollak, D. D. (2015). Anhedonic behavior in cryptochrome 2-deficient mice is paralleled by altered diurnal patterns of amygdala gene expression. Amino Acids, 47(7), pp. 1367-77. doi:10.1007/s00726-015-1968-3.
Savalli G, et al. Anhedonic Behavior in Cryptochrome 2-deficient Mice Is Paralleled By Altered Diurnal Patterns of Amygdala Gene Expression. Amino Acids. 2015;47(7):1367-77. PubMed PMID: 25820768.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Anhedonic behavior in cryptochrome 2-deficient mice is paralleled by altered diurnal patterns of amygdala gene expression. AU - Savalli,Giorgia, AU - Diao,Weifei, AU - Berger,Stefanie, AU - Ronovsky,Marianne, AU - Partonen,Timo, AU - Pollak,Daniela D, Y1 - 2015/03/28/ PY - 2015/01/12/received PY - 2015/03/17/accepted PY - 2015/3/31/entrez PY - 2015/3/31/pubmed PY - 2016/3/5/medline SP - 1367 EP - 77 JF - Amino acids JO - Amino Acids VL - 47 IS - 7 N2 - Mood disorders are frequently paralleled by disturbances in circadian rhythm-related physiological and behavioral states and genetic variants of clock genes have been associated with depression. Cryptochrome 2 (Cry2) is one of the core components of the molecular circadian machinery which has been linked to depression, both, in patients suffering from the disease and animal models of the disorder. Despite this circumstantial evidence, a direct causal relationship between Cry2 expression and depression has not been established. Here, a genetic mouse model of Cry2 deficiency (Cry2 (-/-) mice) was employed to test the direct relevance of Cry2 for depression-like behavior. Augmented anhedonic behavior in the sucrose preference test, without alterations in behavioral despair, was observed in Cry2 (-/-) mice. The novelty suppressed feeding paradigm revealed reduced hyponeophagia in Cry2 (-/-) mice compared to wild-type littermates. Given the importance of the amygdala in the regulation of emotion and their relevance for the pathophysiology of depression, potential alterations in diurnal patterns of basolateral amygdala gene expression in Cry2 (-/-) mice were investigated focusing on core clock genes and neurotrophic factor systems implicated in the pathophysiology of depression. Differential expression of the clock gene Bhlhe40 and the neurotrophic factor Vegfb were found in the beginning of the active (dark) phase in Cry2 (-/-) compared to wild-type animals. Furthermore, amygdala tissue of Cry2 (-/-) mice contained lower levels of Bdnf-III. Collectively, these results indicate that Cry2 exerts a critical role in the control of depression-related emotional states and modulates the chronobiological gene expression profile in the mouse amygdala. SN - 1438-2199 UR - https://www.unboundmedicine.com/medline/citation/25820768/Anhedonic_behavior_in_cryptochrome_2_deficient_mice_is_paralleled_by_altered_diurnal_patterns_of_amygdala_gene_expression_ L2 - https://dx.doi.org/10.1007/s00726-015-1968-3 DB - PRIME DP - Unbound Medicine ER -