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    Involvement of the agmatinergic system in the depressive-like phenotype of the Crtc1 knockout mouse model of depression

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    Type
    Article
    Authors
    Meylan, E M
    Breuillaud, L
    Seredenina, T
    Magistretti, Pierre J. cc
    Halfon, O
    Luthi-Carter, R
    Cardinaux, J-R
    KAUST Department
    Biological and Environmental Sciences and Engineering (BESE) Division
    Bioscience Program
    Date
    2016-07-12
    Online Publication Date
    2016-07-12
    Print Publication Date
    2016-07
    Permanent link to this record
    http://hdl.handle.net/10754/617287
    
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    Abstract
    Recent studies implicate the arginine-decarboxylation product agmatine in mood regulation. Agmatine has antidepressant properties in rodent models of depression, and agmatinase (Agmat), the agmatine-degrading enzyme, is upregulated in the brains of mood disorder patients. We have previously shown that mice lacking CREB-regulated transcription coactivator 1 (CRTC1) associate behavioral and molecular depressive-like endophenotypes, as well as blunted responses to classical antidepressants. Here, the molecular basis of the behavioral phenotype of Crtc1−/− mice was further examined using microarray gene expression profiling that revealed an upregulation of Agmat in the cortex of Crtc1−/− mice. Quantitative polymerase chain reaction and western blot analyses confirmed Agmat upregulation in the Crtc1−/− prefrontal cortex (PFC) and hippocampus, which were further demonstrated by confocal immunofluorescence microscopy to comprise an increased number of Agmat-expressing cells, notably parvalbumin- and somatostatin-positive interneurons. Acute agmatine and ketamine treatments comparably improved the depressive-like behavior of male and female Crtc1−/− mice in the forced swim test, suggesting that exogenous agmatine has a rapid antidepressant effect through the compensation of agmatine deficit because of upregulated Agmat. Agmatine rapidly increased brain-derived neurotrophic factor (BDNF) levels only in the PFC of wild-type (WT) females, and decreased eukaryotic elongation factor 2 (eEF2) phosphorylation in the PFC of male and female WT mice, indicating that agmatine might be a fast-acting antidepressant with N-methyl-D-aspartate (NMDA) receptor antagonist properties. Collectively, these findings implicate Agmat in the depressive-like phenotype of Crtc1−/− mice, refine current understanding of the agmatinergic system in the brain and highlight its putative role in major depression.
    Citation
    Involvement of the agmatinergic system in the depressive-like phenotype of the Crtc1 knockout mouse model of depression 2016, 6 (7):e852 Translational Psychiatry
    Sponsors
    We thank Suzanne Badoux for her initial work with an agmatinase antibody that was not used in this study. This work was funded by a grant from the Swiss National Science Foundation (31003A-135692) and partly supported by the National Centre of Competence in Research (NCCR) Synapsy.
    Publisher
    Springer Nature
    Journal
    Translational Psychiatry
    DOI
    10.1038/tp.2016.116
    Additional Links
    http://www.nature.com/doifinder/10.1038/tp.2016.116
    ae974a485f413a2113503eed53cd6c53
    10.1038/tp.2016.116
    Scopus Count
    Collections
    Articles; Biological and Environmental Sciences and Engineering (BESE) Division; Bioscience Program

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