dc.contributor.author | Gil de la Pisa, Itziar | |
dc.contributor.author | Cebrián, Carolina | |
dc.contributor.author | Ortega Calvo, Jorge | |
dc.contributor.author | Meana Martínez, José Javier | |
dc.contributor.author | Sulzer, David | |
dc.date.accessioned | 2015-12-02T15:08:35Z | |
dc.date.available | 2015-12-02T15:08:35Z | |
dc.date.issued | 2014-07-29 | |
dc.identifier.citation | Journal of Neuroinflammation 11 : (2014) // Article ID 128 | es |
dc.identifier.issn | 1742-2094 | |
dc.identifier.uri | http://hdl.handle.net/10810/16303 | |
dc.description.abstract | Background: An accumulating body of evidence points to the significance of neuroinflammation and immunogenetics in schizophrenia, and an imbalance of cytokines in the central nervous system (CNS) has been suggested to be associated with the disorder. Munc18-overexpressing mice (Munc18-OE) have provided a model for the study of the alterations that may underlie the symptoms of subjects with schizophrenia. The aim of the present study was to elucidate the involvement of neuroinflammation and cytokine imbalance in this model.
Methods: Cytokines were evaluated in the cortex and the striatum of Munc18-OE and wild-type (WT) mice by enzyme-linked immunosorbent assay (ELISA). Protein levels of specific microglia and macrophage, astrocytic and neuroinflammation markers were quantified by western blot in the cortex and the striatum of Munc18-OE and WT mice.
Results: Each cytokine evaluated (Interferon-gamma (IFN-gamma), Tumor Necrosis Factor-alpha (TNF-alpha), Interleukin-2 (IL-2) and CCL2 chemokine) was present at higher levels in the striatum of Munc18-OE mice than WT. Cortical TNF-alpha and IL-2 levels were significantly lower in Munc18-OE mice than WT mice. The microglia and macrophage marker CD11b was lower in the cortexes of Munc18-OE mice than WT, but no differences were observed in the striatum. Glial Fibrillary Acidic Protein (GFAP) and Nuclear Factor-kappaB (NF-kappa B)p65 levels were not different between the groups. Interleukin-1beta (IL-1 beta) and IL-6 levels were beneath detection limits.
Conclusions: The disrupted levels of cytokines detected in the brain of Munc18-OE mice was found to be similar to clinical reports and endorses study of this type for analysis of this aspect of the disorder. The lower CD11b expression in the cortex but not in the striatum of the Munc18-OE mice may reflect differences in physiological activity. The cytokine expression pattern observed in Munc18-OE mice is similar to a previously published model of schizophrenia caused by maternal immune activation. Together, these data suggest a possible role for an immune imbalance in this disorder. | es |
dc.description.sponsorship | The study was supported by Spanish MINECO (SAF2009-08460) and the Basque Government (IT616-13) to JJM. Experiments were performed in DS's laboratory. CC was supported by the Caja Madrid Foundation and the Parkinson's Disease Foundation. DS's laboratory was supported by NIDA07418 and DA10154 and the Parkinson's, Simons and JPB Foundations. | es |
dc.language.iso | eng | es |
dc.publisher | Biomed Central | es |
dc.relation | info:eu-repo/grantAgreement/MINECO/SAF2009-08460 | |
dc.rights | info:eu-repo/semantics/openAccess | es |
dc.subject | Munc18-1a | es |
dc.subject | animal model | es |
dc.subject | schizophrenia | es |
dc.subject | neuroinflammation | es |
dc.subject | cytokine | es |
dc.subject | central-nervous-system | es |
dc.subject | prefrontal cortex | es |
dc.subject | inflammatory cytokines | es |
dc.subject | psichiatric-disorders | es |
dc.subject | inmune activation | es |
dc.subject | dopamine | es |
dc.subject | metaanalysis | es |
dc.subject | hypofrontality | es |
dc.subject | hypothesis | es |
dc.subject | release | es |
dc.title | Cytokine pathway disruption in a mouse model of schizophrenia induced by Munc18-1a overexpression in the brain | es |
dc.type | info:eu-repo/semantics/article | es |
dc.rights.holder | © 2014 Gil-Pisa et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain
Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article,
unless otherwise stated. | es |
dc.relation.publisherversion | http://www.jneuroinflammation.com/content/11/1/128#abs | es |
dc.identifier.doi | 10.1186/1742-2094-11-128 | |
dc.departamentoes | Farmacología | es_ES |
dc.departamentoeu | Farmakologia | es_ES |
dc.subject.categoria | CELLULAR AND MOLECULAR NEUROSCIENCE | |
dc.subject.categoria | NEUROLOGY | |
dc.subject.categoria | IMMUNOLOGY AND MICROBIOLOGY | |