Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetite
Autor(a) principal: | |
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Data de Publicação: | 2002 |
Outros Autores: | , , , |
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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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 |
|
_version_ |
1797789400749309952 |