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Regulation of markers of synaptic function in mouse models of depression: chronic mild stress and decreased expression of VGLUT1
Autor(es) : Elizalde, N. (N.)
Pastor, P.M. (Pedro M.)
Garcia-Garcia, A.L. (A.L.)
Serres, F. (F.)
Venzala, E. (E.)
Huarte, J. (J.)
Ramirez, M.J. (María Javier)
Rio, J. (Joaquín) del
Sharp, T. (T.)
Tordera, R.M. (Rosa María)
Palabras clave : Synaptic vesicle protein
Major depression
BDNF
Arc
Synapsin 1
Fecha incorporación: 2010
Editorial : Wiley Blackwell
Versión del editor: http://dx.doi.org/10.1111/j.1471-4159.2010.06854.x
ISSN: 0022-3042
Cita: Elizalde N, Pastor PM, Garcia-Garcia AL, Serres F, Venzala E, Huarte J, et al. Regulation of markers of synaptic function in mouse models of depression: chronic mild stress and decreased expression of VGLUT1. J Neurochem 2010 Sep 1;114(5):1302-1314.
Resumen
Depression has been linked to failure in synaptic plasticity originating from environmental and/or genetic risk factors. The chronic mild stress (CMS) model regulates the expression of synaptic markers of neurotransmitter function and associated depressive-like behaviour. Moreover, 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, mechanisms of failure in synaptic plasticity, common to stress and impaired glutamate function. First, we show that CMS induced a transient decrease of different plasticity markers (VGLUT1, synapsin 1, sinaptophysin, rab3A and activity regulated cytoskeletal protein Arc) but a long-lasting decrease of the brain derived neurotrophic factor (BDNF) as well as depressive-like behaviour. The immediate early gene (IEG) Arc was also downregulated in VGLUT1+/- heterozygous mice. In contrast, an opposite regulation of synapsin 1 was observed. Finally, both models showed a marked increase of cortical Arc response to novelty. Increased Arc response to novelty could be suggested as a molecular mechanism underlying failure to adapt to environmental changes, common to chronic stress and altered glutamate function. Further studies should investigate whether these changes are associated to depressive-like behaviour both in animal models and in depressed patients.
Enlace permanente: http://hdl.handle.net/10171/17210
Aparece en las colecciones: DA - CIMA - Neurociencias - Neurofarmacología y conducta - Artículos de Revista
DA - Farmacia - Farmacología - Artículos de revista

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