Mecanismos prosencefálicos envolvidos na ingestão de sódio e água induzida pela ativação gabaérgica do núcleo parabraquial lateral
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Data
2010-06-29
Autores
Roncari, Camila Ferreira [UNESP]
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Editor
Universidade Estadual Paulista (Unesp)
Resumo
Estudos recentes mostraram a existência de importantes mecanismos de controle da ingestão de sódio e água no núcleo parabraquial lateral (NPBL), uma estrutura pontina localizada dorsolateralmente ao pedúnculo cerebelar superior. Lesões eletrolíticas ou neurotóxicas do NPBL aumentam a ingestão de água induzida por administração central ou periférica de angiotensina II (ANG II). O bloqueio dos receptores serotoninérgicos, colecistocinérgicos ou glutamatérgicos com injeções bilaterais no NPBL de metisergida, proglumide ou DNQX, respectivamente, aumentam a ingestão de solução hipertônica de NaCl induzida por tratamento com o diurético furosemida combinado com doses baixas do inibidor da enzima conversora de angiotensina captopril injetados subcutaneamente. Metisergida injetada no NPBL ainda aumenta a ingestão de NaCl induzida por ANG II administrada no ventrículo lateral (VL) ou no órgão subfornical (OSF) e por privação hídrica por 24 h, depleção de sódio ou DOCA. Além disso, a ativação de receptores adrenérgicos a2 com injeções de moxonidina ou noradrenalina no NPBL aumenta a ingestão de NaCl induzida por furosemida + captopril. Sendo assim, esses estudos mostram que o bloqueio dos mecanismos inibitórios do NPBL com injeções de antagonistas de receptores serotoninérgicos, colecistocinérgicos e glutamatérgicos ou agonistas de receptores adrenérgicos aumenta a ingestão de NaCl e água induzida por tratamentos prévios. No entanto, mais recentemente mostrou-se que a ativação gabaérgica do NPBL induz ingestão de NaCl e água em ratos saciados e normovolêmicos que não receberam nenhum tratamento prévio. Essa resposta é reduzida pelo bloqueio dos mecanismos colinérgicos centrais. No presente estudo, investigamos o efeito da desativação de mecanismos prosencefálicos facilitatórios na ingestão de NaCl e água induzida pela ativação gabaérgica...
Recent studies have shown important mechanisms for the control of sodium and water intake in the lateral parabrachial nucleus (LPBN), a pontine structure localized dorsolaterally to the superior cerebellar peduncle. Electrolytic or neurotoxic lesions of the LPBN increase water intake induced by central or peripheral administration of angiotensin II (ANG II). The blockade of serotonergic, cholecystokinergic or glutamatergic receptors with bilateral injections of methysergide, proglumide or DNQX, respectively, into the LPBN increases hypertonic NaCl intake induced by the treatment with subcutaneous injections of diuretic furosemide combined with low dose of angiotensin converting enzyme inhibitor captopril. LPBN injections of methysergide also increases NaCl intake induced by ANG II injected in the lateral ventricle (LV) or into the subfornical organ (SFO) and 24 h water deprivation, sodium depletion or DOCA. Moreover, activation of α2-adrenoceptors with injections of moxonidine or noradrenaline into the LPBN also increases NaCl intake induced by furosemide + captopril. Therefore theses studies have shown that blockade of LPBN inhibitory mechanisms with injections of serotonergic, cholecystokinergic or glutamatergic antagonists or adrenergic agonists increase NaCl and water intake induced by treatments that induce water and/or NaCl intake. However, recently it has been shown that GABAergic activation of the LPBN induces NaCl and water intake in satiated and normovolemic rats that received no previous treatment, a response reduced by the blockade of central cholinergic mechanisms. In the present study, we investigated the effects of deactivation of forebrain facilitatory mechanisms on NaCl and water intake induced by gabaergic activation of the LPBN. Rats with stainless steel cannulas implanted into the LV or SFO and bilaterally into the LPBN were used to test the effects of the blockade... (Complete abstract click electronic access below)
Recent studies have shown important mechanisms for the control of sodium and water intake in the lateral parabrachial nucleus (LPBN), a pontine structure localized dorsolaterally to the superior cerebellar peduncle. Electrolytic or neurotoxic lesions of the LPBN increase water intake induced by central or peripheral administration of angiotensin II (ANG II). The blockade of serotonergic, cholecystokinergic or glutamatergic receptors with bilateral injections of methysergide, proglumide or DNQX, respectively, into the LPBN increases hypertonic NaCl intake induced by the treatment with subcutaneous injections of diuretic furosemide combined with low dose of angiotensin converting enzyme inhibitor captopril. LPBN injections of methysergide also increases NaCl intake induced by ANG II injected in the lateral ventricle (LV) or into the subfornical organ (SFO) and 24 h water deprivation, sodium depletion or DOCA. Moreover, activation of α2-adrenoceptors with injections of moxonidine or noradrenaline into the LPBN also increases NaCl intake induced by furosemide + captopril. Therefore theses studies have shown that blockade of LPBN inhibitory mechanisms with injections of serotonergic, cholecystokinergic or glutamatergic antagonists or adrenergic agonists increase NaCl and water intake induced by treatments that induce water and/or NaCl intake. However, recently it has been shown that GABAergic activation of the LPBN induces NaCl and water intake in satiated and normovolemic rats that received no previous treatment, a response reduced by the blockade of central cholinergic mechanisms. In the present study, we investigated the effects of deactivation of forebrain facilitatory mechanisms on NaCl and water intake induced by gabaergic activation of the LPBN. Rats with stainless steel cannulas implanted into the LV or SFO and bilaterally into the LPBN were used to test the effects of the blockade... (Complete abstract click electronic access below)
Descrição
Palavras-chave
Orgão subfornical, Angiotensina, Muscimol, Acetilcolina, Muscimol, Angiotensin II, Acetylcholine, Subfornical organ
Como citar
RONCARI, Camila Ferreira. Mecanismos prosencefálicos envolvidos na ingestão de sódio e água induzida pela ativação gabaérgica do núcleo parabraquial lateral. 2010. 72 f. Dissertação (mestrado) - UNESP/UFSCar, Programa Interinstitucional de Pós-Graduação em Ciências Fisiológicas, 2010.