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dc.contributor.authorGarcía, Ana P.es
dc.contributor.authorAitta-aho, Teemues
dc.contributor.authorSchaaf, Lauraes
dc.contributor.authorHeeley, Nicholases
dc.contributor.authorHeuschmid, Lenaes
dc.contributor.authorBai, Yunjinges
dc.contributor.authorBarrantes, Francisco Josées
dc.contributor.authorApergis-Schoute, Johnes
dc.date.accessioned2019-09-13T13:19:29Z-
dc.date.available2019-09-13T13:19:29Z-
dc.date.issued2015-
dc.identifier.citationGarcía AP, Aitta-aho T, Schaaf L, Heeley N, Heuschmid L, Bai Y, et al. (2015) Nicotinic α4 Receptor-Mediated Cholinergic Influences on Food Intake and Activity Patterns in Hypothalamic Circuits. PLoS ONE 10(8): e0133327. doi:10.1371/journal.pone.0133327. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8735es
dc.identifier.issn1932-6203 (online)-
dc.identifier.urihttps://repositorio.uca.edu.ar/handle/123456789/8735-
dc.description.abstractAbstract: Nicotinic acetylcholine receptors (nAChRs) play an important role in regulating appetite and have been shown to do so by influencing neural activity in the hypothalamus. To shed light on the hypothalamic circuits governing acetylcholine's (ACh) regulation of appetite this study investigated the influence of hypothalamic nAChRs expressing the α4 subunit. We found that antagonizing the α4β2 nAChR locally in the lateral hypothalamus with di-hydro-ß-erythroidine (DHβE), an α4 nAChR antagonist with moderate affinity, caused an increase in food intake following free access to food after a 12 hour fast, compared to saline-infused animals. Immunocytochemical analysis revealed that orexin/hypocretin (HO), oxytocin, and tyrosine hydroxylase (TH)-containing neurons in the A13 and A12 of the hypothalamus expressed the nAChR α4 subunit in varying amounts (34%, 42%, 50%, and 51%, respectively) whereas melanin concentrating hormone (MCH) neurons did not, suggesting that DHβE-mediated increases in food intake may be due to a direct activation of specific hypothalamic circuits. Systemic DHβE (2 mg/kg) administration similarly increased food intake following a 12 hour fast. In these animals a subpopulation of orexin/hypocretin neurons showed elevated activity compared to control animals and MCH neuronal activity was overall lower as measured by expression of the immediate early gene marker for neuronal activity cFos. However, oxytocin neurons in the paraventricular hypothalamus and TH-containing neurons in the A13 and A12 did not show differential activity patterns. These results indicate that various neurochemically distinct hypothalamic populations are under the influence of α4β2 nAChRs and that cholinergic inputs to the lateral hypothalamus can affect satiety signals through activation of local α4β2 nAChR-mediated transmission.es
dc.formatapplication/pdfes
dc.language.isoenges
dc.publisherPublic Library of Sciencees
dc.rightsAcceso abierto*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.sourcePLoS ONE Vol. 10, N° 8, 2015es
dc.subjectMEDICINAes
dc.subjectRECEPTORESes
dc.subjectREGULACION DEL APETITOes
dc.subjectHIPOTALAMOes
dc.subjectNEURONASes
dc.titleNicotinic α4 receptor-mediated cholinergic influences on food intake and activity patterns in hypothalamic circuitses
dc.typeArtículoes
dc.identifier.doi10.1371/journal.pone.0133327-
dc.identifier.pmid26247203-
uca.disciplinaMEDICINAes
uca.issnrd1es
uca.affiliationFil: Garcia, Ana P. University of Cambridge. Department of Pharmacology; Reino Unidoes
uca.affiliationFil: García, Ana P. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Neurobiología Molecular; Argentinaes
uca.affiliationFil: García, Ana P. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.affiliationFil: Aitta-aho, Teemu. University of Cambridge. Department of Pharmacology; Reino Unidoes
uca.affiliationFil: Schaaf, Laura. University of Cambridge. Department of Pharmacology; Reino Unidoes
uca.affiliationFil: Heeley, Nicholas. University of Cambridge. Institute of Metabolic Science; Reino Unidoes
uca.affiliationFil: Heuschmid, Lena. University of Cambridge. Department of Pharmacology; Reino Unidoes
uca.affiliationFil: Bai, Yunjing. Chinese Academy of Sciences. Key Laboratory of Mental Health, Institute of Psychology; Chinaes
uca.affiliationFil: Barrantes, Francisco José. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Neurobiología Molecular; Argentinaes
uca.affiliationFil: Barrantes, Francisco José. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.affiliationFil: Apergis-Schoute, John. University of Cambridge. Department of Pharmacology; Reino Unidoes
uca.affiliationFil: Apergis-Schoute, John. University of Cambridge. Institute of Metabolic Science; Reino Unidoes
uca.versionpublishedVersiones
item.grantfulltextopen-
item.fulltextWith Fulltext-
item.languageiso639-1en-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.deptLaboratorio de Neurobiología Molecular-
crisitem.author.deptFacultad de Ciencias Médicas-
crisitem.author.orcid0000-0002-4745-681X-
crisitem.author.parentorgFacultad de Ciencias Médicas-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.parentorgPontificia Universidad Católica Argentina-
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