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

Detalhes bibliográficos
Autor(a) principal: Menani, José Vanderlei [UNESP]
Data de Publicação: 2002
Outros Autores: Barbosa, S. P., De Luca, L. A., De Gobbi, JIF, Johnson, A. K.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://ajpregu.physiology.org/content/282/3/R837
http://hdl.handle.net/11449/32542
Resumo: Central 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 mug), 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.
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spelling Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetitecarbacholwater intakethirstsalt intakesalt appetite5-hydroxytryptamineCentral 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 mug), 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.Univ Iowa, Dept Psychol, Iowa City, IA 52242 USAUniv Iowa, Dept Pharmacol & Exercise Sci, Iowa City, IA 52242 USAUniv Iowa, Ctr Cardiovasc, Iowa City, IA 52242 USAPaulista State Univ, Dept Physiol & Pathol, Sch Dent, BR-14801903 São Paulo, BrazilPaulista State Univ, Dept Physiol & Pathol, Sch Dent, BR-14801903 São Paulo, BrazilAmer Physiological SocUniv IowaUniversidade Estadual Paulista (Unesp)Menani, José Vanderlei [UNESP]Barbosa, S. P.De Luca, L. A.De Gobbi, JIFJohnson, A. K.2014-05-20T15:21:23Z2014-05-20T15:21:23Z2002-03-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleR837-R841http://ajpregu.physiology.org/content/282/3/R837American Journal of Physiology-regulatory Integrative and Comparative Physiology. Bethesda: Amer Physiological Soc, v. 282, n. 3, p. R837-R841, 2002.0363-6119http://hdl.handle.net/11449/32542WOS:0001737792000261023597870118105Web of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengAmerican Journal of Physiology: Regulatory Integrative and Comparative Physiology3.0821,550info:eu-repo/semantics/openAccess2021-10-23T10:36:56Zoai:repositorio.unesp.br:11449/32542Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462021-10-23T10:36:56Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetite
title Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetite
spellingShingle Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetite
Menani, José Vanderlei [UNESP]
carbachol
water intake
thirst
salt intake
salt appetite
5-hydroxytryptamine
title_short Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetite
title_full Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetite
title_fullStr Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetite
title_full_unstemmed Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetite
title_sort Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetite
author Menani, José Vanderlei [UNESP]
author_facet Menani, José Vanderlei [UNESP]
Barbosa, S. P.
De Luca, L. A.
De Gobbi, JIF
Johnson, A. K.
author_role author
author2 Barbosa, S. P.
De Luca, L. A.
De Gobbi, JIF
Johnson, A. K.
author2_role author
author
author
author
dc.contributor.none.fl_str_mv Univ Iowa
Universidade Estadual Paulista (Unesp)
dc.contributor.author.fl_str_mv Menani, José Vanderlei [UNESP]
Barbosa, S. P.
De Luca, L. A.
De Gobbi, JIF
Johnson, A. K.
dc.subject.por.fl_str_mv carbachol
water intake
thirst
salt intake
salt appetite
5-hydroxytryptamine
topic carbachol
water intake
thirst
salt intake
salt appetite
5-hydroxytryptamine
description Central 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 mug), 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.
publishDate 2002
dc.date.none.fl_str_mv 2002-03-01
2014-05-20T15:21:23Z
2014-05-20T15:21:23Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://ajpregu.physiology.org/content/282/3/R837
American Journal of Physiology-regulatory Integrative and Comparative Physiology. Bethesda: Amer Physiological Soc, v. 282, n. 3, p. R837-R841, 2002.
0363-6119
http://hdl.handle.net/11449/32542
WOS:000173779200026
1023597870118105
url http://ajpregu.physiology.org/content/282/3/R837
http://hdl.handle.net/11449/32542
identifier_str_mv American Journal of Physiology-regulatory Integrative and Comparative Physiology. Bethesda: Amer Physiological Soc, v. 282, n. 3, p. R837-R841, 2002.
0363-6119
WOS:000173779200026
1023597870118105
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv American Journal of Physiology: Regulatory Integrative and Comparative Physiology
3.082
1,550
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv R837-R841
dc.publisher.none.fl_str_mv Amer Physiological Soc
publisher.none.fl_str_mv Amer Physiological Soc
dc.source.none.fl_str_mv Web of Science
reponame:Repositório Institucional da UNESP
instname:Universidade Estadual Paulista (UNESP)
instacron:UNESP
instname_str Universidade Estadual Paulista (UNESP)
instacron_str UNESP
institution UNESP
reponame_str Repositório Institucional da UNESP
collection Repositório Institucional da UNESP
repository.name.fl_str_mv Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)
repository.mail.fl_str_mv
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