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Chronic stress and impaired glutamate function elicit a depressive-like phenotype and common changes in gene expression in the mouse frontal cortex
Autor(es) : Tordera, R.M. (Rosa María)
Garcia-Garcia, A.L. (A.L.)
Elizalde, N. (N.)
Segura, V. (Víctor)
Aso, E. (E.)
Venzala, E. (E.)
Ramirez, M.J. (María Javier)
Rio, J. (Joaquín) del
Palabras clave : Chronic mild stress
VGLUT1
Major depression
Animal models
Gene expression
Fecha incorporación: 2011
Editorial : Elservier
Versión del editor: http://dx.doi.org/10.1016/j.euroneuro.2010.06.016
ISSN: 0924-977X
Cita: Tordera RM, Garcia-Garcia AL, Elizalde N, Segura V, Aso E, Venzala E, et al. Chronic stress and impaired glutamate function elicit a depressive-like phenotype and common changes in gene expression in the mouse frontal cortex. Eur Neuropsychopharmacol 2011 Jan;21(1):23-32.
Resumen
Major depression might originate from both environmental and genetic risk factors. The environmental chronic mild stress (CMS) model mimics some environmental factors contributing to human depression and induces anhedonia and helplessness. Mice heterozygous for the synaptic vesicle protein (SVP) vesicular glutamate transporter 1 (VGLUT1) have been proposed as a genetic model of deficient glutamate function linked to depressive-like behaviour. Here, we aimed to identify, in these two experimental models, gene expression changes in the frontal cortex, common to stress and impaired glutamate function. Both VGLUT1+/- and CMS mice showed helpless and anhedonic-like behavior. Microarray studies in VGLUT1+/- mice revealed regulation of genes involved in apoptosis, neurogenesis, synaptic transmission, protein metabolic process or learning and memory. In addition, RT-PCR studies confirmed gene expression changes in several glutamate, GABA, dopamine and serotonin neurotransmitter receptors. On the other hand, CMS affected the regulation of 147 transcripts, some of them involved in response to stress and oxidoreductase activity. Interestingly, 52 genes were similarly regulated in both models. Specifically, a dowregulation in genes that promote cell proliferation (Anapc7), cell growth (CsnK1g1), cell survival (Hdac3), inhibition of apoptosis (Dido1) was observed. Genes linked to cytoskeleton (Hspg2, Invs), psychiatric disorders (Grin1, MapK12) or an antioxidant enzyme (Gpx2) were also downregulated. Moreover, genes that inhibit the MAPK pathways (Dusp14), stimulate oxidative metabolism (Eif4a2) and enhance glutamate transmission (Rab8b) were upregulated. We suggest that these genes could form part of the altered “molecular context” underlying depressive-like behaviour in animal models. The clinical relevance of these findings is discussed.
Enlace permanente: http://hdl.handle.net/10171/17249
Aparece en las colecciones: DA - CIMA - Neurociencias - Neurofarmacología y conducta - Artículos de Revista
DA - Farmacia - Farmacología - Artículos de revista

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