Ghrelin activates hypophysiotropic corticotropin-releasing factor neurons independently of the arcuate nucleus

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dc.contributor.affiliationLaboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology [IMBICE-Argentine Research Council (CONICET) and Scientific Research Commission, Province of Buenos Aires (CIC-PBA)], La Plata, Buenos Aires, Argentinaes_ES
dc.contributor.emailmarioperello@yahoo.comes_ES
dc.creatorCabral, Agustina
dc.creatorPortiansky, Enrique
dc.creatorSánchez-Jaramillo, Edith
dc.creatorZigman, Jeffrey M.
dc.creatorPerello, Mario
dc.creator.identificador"SAJE691113MHGNRD06">Sánchez Jaramillo, Edithes_ES
dc.date.accessioned2017-06-29T03:50:44Z
dc.date.accessioned2026-03-27T14:33:02Z
dc.date.available2017-06-29T03:50:44Z
dc.date.issued2016es_ES
dc.date.published2016es_ES
dc.description.abstractotrodiomaPrevious work has established that the hormone ghrelin engages the hypothalamic–pituitary–adrenal neuroendocrine axis via activation of corticotropin-releasing factor (CRF) neurons of the hypothalamic paraventricular nucleus (PVN). The neuronal circuitry that mediates this effect of ghrelin is currently unknown. Here, we show that ghrelin-induced activation of PVN CRF neurons involved inhibition of -aminobutyric acid (GABA) inputs, likely via ghrelin binding sites that were localized at GABAergic terminals within the PVN. While ghrelin activated PVN CRF neurons in the presence of neuropeptide Y (NPY) receptor antagonists or in arcuate nucleus (ARC)-ablated mice, it failed to do it so in mice with ghrelin receptor expression limited to ARC agouti gene related protein (AgRP)/NPY neurons. These data support the notion that ghrelin activates PVN CRF neurons via inhibition of local GABAergic tone, in an ARC-independent manner. Furthermore,these data suggestthatthe neuronal circuits mediating ghrelin’s orexigenic action vs. its role as a stress signal are anatomically dissociated.es_ES
dc.description.monthMayes_ES
dc.identifier2733es_ES
dc.identifier.citationMercedes Simoni Nieveses_ES
dc.identifier.doi10.1016/j.psyneuen.2016.01.027es_ES
dc.identifier.eissn1873-3360es_ES
dc.identifier.issn0306-4530es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.identifier.paginacion27-39es_ES
dc.identifier.placeInglaterraes_ES
dc.identifier.urihttps://doi.org/10.1016/j.psyneuen.2016.01.027es_ES
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4808343/es_ES
dc.identifier.urihttps://repositorio.inprf.gob.mx/handle/123456789/4582
dc.identifier.volumen67es_ES
dc.language.isoenges_ES
dc.publisherPergamon Presses_ES
dc.relation67:27-39es_ES
dc.relation.jnabreviadoPSYCHONEUROENDOCRINOLOGYes_ES
dc.relation.journalPsychoneuroendocrinologyes_ES
dc.rightsAcceso Cerradoes_ES
dc.subject.koStresses_ES
dc.subject.koGhrelin Orexigenices_ES
dc.subject.koAminobutyric acid (GABA)es_ES
dc.subject.koNeuropeptide Y (NPY)es_ES
dc.subject.kwStress
dc.subject.kwGhrelin
dc.subject.kwOrexigenic
dc.subject.kwγ-Aminobutyric acid (GABA)
dc.subject.kwNeuropeptide Y (NPY)
dc.titleGhrelin activates hypophysiotropic corticotropin-releasing factor neurons independently of the arcuate nucleuses_ES
dc.typeArtículoes_ES

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