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Mitogen-Activated Protein Kinase Contributes to Lipopolysaccharide-Induced Activation of Corticotropin-Releasing Hormone Synthesizing Neurons in the Hypothalamic Paraventricular Nucleus

dc.creatorSingru, Praful S.
dc.creatorSánchez, Edith
dc.creatorAcharya, Runa
dc.creatorFekete, Csaba
dc.creatorLechan, Ronald M.
dc.date.accessioned2017-06-30T03:42:10Z
dc.date.available2017-06-30T03:42:10Z
dc.date.issued2008es_ES
dc.identifier2130es_ES
dc.identifier.issn0013-7227es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/6788
dc.identifier.urihttps://doi.org/10.1210/en.2007-1478es_ES
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2329264/es_ES
dc.language.isoenges_ES
dc.publisherThe Endocrine Societyes_ES
dc.relation149 (5) 2283–2292 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.titleMitogen-Activated Protein Kinase Contributes to Lipopolysaccharide-Induced Activation of Corticotropin-Releasing Hormone Synthesizing Neurons in the Hypothalamic Paraventricular Nucleuses_ES
dc.typearticlees_ES
dc.contributor.affiliationTupper Research Institute and Department of Medicine Division of Endocrinology, Diabetes, and Metabolism, Tufts-New England Medical Center, Boston, Massachusetts 02111; Department of Endocrine Neurobiologyes_ES
dc.relation.jnabreviadoENDOCRINOLOGYes_ES
dc.relation.journalEndocrinologyes_ES
dc.identifier.placeEstados Unidoses_ES
dc.date.published2008es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.identifier.doi10.1210/en.2007-1478es_ES
dc.description.monthMayes_ES
dc.description.abstractotrodiomaTo determine whether the p44/p42 MAPK (ERK1/2) signaling pathway is involved in the activation of CRH-containing neurons in the hypothalamic paraventricular nucleus (PVN) after bacterial lipopolysaccharide (LPS) administration, Sprague Dawley rats were injected with LPS, and studied after 2, 6, 9, and 12 h. In saline-treated controls, isolated weak phosphorylated (phospho)ERK1/2 immunoreactive neurons were observed in the PVN. However, a dramatic increase in phospho- ERK1/2 immunoreactivity was apparent in the PVN 2 h after LPS administration, and gradually declined to baseline levels 9–12 h after injection. By double-labeling immunofluorescence, all CRH-containing neurons in the PVN contained phospho-ERK1/2 2 h after LPS. Intracerebroventricular administration of the MAPK inhibitor, PD98059, prevented LPSinduced ERK1/2 phosphorylation, c-fos activation, and the increase of CRH gene expression in the PVN but had no effect on c-fos activation in brainstem A2-C1/C2 regions. We conclude that LPS rapidly increases the phospho-ERK1/2 in CRHcontaining neurons in the PVN and that activation of MAPKs is necessary for LPS-induced activation of the hypothalamicpituitary- adrenal axises_ES


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