Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetite

Página do item simplificado
dc.contributor.authorMenani, José Vanderlei [UNESP]
dc.contributor.authorBarbosa, Silas Pereira [UNESP]
dc.contributor.authorDe Luca Jr., Laurival Antonio [UNESP]
dc.contributor.authorDe Gobbi, Juliana Irani Fratucci [UNESP]
dc.contributor.authorJohnson, Alan Kim [UNESP]
dc.contributor.institutionUniversity of Iowa
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.contributor.institution11 Seashore Hall E
dc.date.accessioned2022-04-28T19:55:27Z
dc.date.available2022-04-28T19:55:27Z
dc.date.issued2002-01-01
dc.description.abstractCentral cholinergic mechanisms are suggested to participate in osmoreceptor-induced water intake. Therefore, central injections of the cholinergic agonist carbachol usually produce water intake (i.e., thirst) and are ineffective in inducing the intake of hypertonic saline solutions (i.e., the operational definition of sodium appetite). Recent studies have indicated that bilateral injections of the serotonin receptor antagonist methysergide into the lateral parabrachial nucleus (LPBN) markedly increases salt intake in models involving the activation of the renin-angiotensin system or mineralocorticoid hormones. The present studies investigated whether sodium appetite could be induced by central cholinergic activation with carbachol (an experimental condition where only water is typically ingested) after the blockade of LPBN serotonergic mechanisms with methysergide treatment in rats. When administered intracerebroventricularly in combination with injections of vehicle into both LPBN, carbachol (4 nmol) caused water drinking but insignificant intake of hypertonic saline. In contrast, after bilateral LPBN injections of methysergide (4 μg), intracerebroventricular carbachol induced the intake of 0.3 M NaCl. Water intake stimulated by intracerebroventricular carbachol was not changed by LPBN methysergide injections. The results indicate that central cholinergic activation can induce marked intake of hypertonic NaCl if the inhibitory serotonergic mechanisms of the LPBN are attenuated.en
dc.description.affiliationDepartment of Psychology Pharmacology and Exercise Science Cardiovascular Center University of Iowa, Iowa City, IA 52242-1407
dc.description.affiliationDepartment of Physiology and Pathology School of Dentistry Paulista State University, Araraquara, Sao Paulo 14801-903
dc.description.affiliationDept. of Psychology Univ. of Iowa 11 Seashore Hall E, Iowa City, IA 52242-1407
dc.description.affiliationUnespDepartment of Physiology and Pathology School of Dentistry Paulista State University, Araraquara, Sao Paulo 14801-903
dc.identifierhttp://dx.doi.org/10.1152/ajpregu.00311.2001
dc.identifier.citationAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology, v. 282, n. 3 51-3, 2002.
dc.identifier.doi10.1152/ajpregu.00311.2001
dc.identifier.issn0363-6119
dc.identifier.scopus2-s2.0-0036083519
dc.identifier.urihttp://hdl.handle.net/11449/224236
dc.language.isoeng
dc.relation.ispartofAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
dc.sourceScopus
dc.subject5-Hydroxytryptamine
dc.subjectCarbachol
dc.subjectSalt appetite
dc.subjectSalt intake
dc.subjectThirst
dc.subjectWater intake
dc.titleSerotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetiteen
dc.typeArtigo

Arquivos

Coleções

Artigos - Fisiologia e Patologia - FOAR