Journal article
Activation of serotonergic 5-HT1A receptors in the lateral parabrachial nucleus increases NaCl intake
Brain research, Vol.1066(1-2), pp.1-9
2005
DOI: 10.1016/j.brainres.2005.04.055
PMID: 16360657
Abstract
Previous studies using non-specific serotonergic agonists and antagonists have shown the importance of serotonergic inhibitory mechanisms in the lateral parabrachial nucleus (LPBN) for controlling sodium and water intake. In the present study, we investigated whether the serotonergic 5-HT1A receptor subtype in the LPBN participates in this control. Male Holtzman rats had cannulas implanted bilaterally into the LPBN. Bilateral injections of the 5-HT1A receptor agonist, 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT, 0.1, 1.25, and 2.5 μg/0.2 μl), into the LPBN enhanced 0.3 M NaCl and water intake of rats injected subcutaneously with the diuretic furosemide (10 mg/kg bw) and a low dose of the angiotensin-converting enzyme inhibitor, captopril (5 mg/kg bw). The increase in NaCl intake produced by 8-OH-DPAT injections was reduced in dose-related manner by pre-treating the LPBN with the selective 5-HT1A serotonergic antagonist, WAY-100635 (WAY, 1 and 2 μg/0.2 μl). In contrast, WAY did not affect water intake produced by 8-OH-DPAT. WAY-100635 injected alone into the LPBN had no effect on NaCl ingestion. Injections of 8-OH-DAPT (0.1 μg/0.2 μl) into the LPBN also increased 0.3 M NaCl intake induced by 24-h sodium depletion (furosemide, 20 mg/kg bw plus 24 h of sodium-free diet). Serotonin (5-HT, 20 μg/0.2 μl) injected alone or combined with 8-OH-DPAT into the LPBN reduced 24-h sodium depletion-induced 0.3 M NaCl intake. Therefore, the activation of serotonergic 5-HT1A receptors in the LPBN increases stimulated hypertonic NaCl and water intake, while 5-HT injections into the LPBN reduce NaCl intake and prevent the effects of serotonergic 5-HT1A receptor activation.
Details
- Title: Subtitle
- Activation of serotonergic 5-HT1A receptors in the lateral parabrachial nucleus increases NaCl intake
- Creators
- Juliana Irani Fratucci De Gobbi - Department of Physiology and Pathology, School of Dentistry, Paulista State University (UNESP), Rua Humaitá, 1680, 14801-903 Araruquara, SP, BrazilSilas P Barbosa - Department of Physiology and Pathology, School of Dentistry, Paulista State University (UNESP), Rua Humaitá, 1680, 14801-903 Araruquara, SP, BrazilLaurival A DE LUCA - Department of Physiology and Pathology, School of Dentistry, Paulista State University (UNESP), Rua Humaitá, 1680, 14801-903 Araruquara, SP, BrazilRobert L Thunhorst - Department of Psychology, University of Iowa, 11 Seashore Hall E, Iowa City, IA 52242-1407, United StatesAllan Kim Johnson - Department of Psychology, University of Iowa, 11 Seashore Hall E, Iowa City, IA 52242-1407, United StatesJosé VANDERLEI MENANI - Department of Physiology and Pathology, School of Dentistry, Paulista State University (UNESP), Rua Humaitá, 1680, 14801-903 Araruquara, SP, Brazil
- Resource Type
- Journal article
- Publication Details
- Brain research, Vol.1066(1-2), pp.1-9
- Publisher
- Elsevier
- DOI
- 10.1016/j.brainres.2005.04.055
- PMID
- 16360657
- ISSN
- 0006-8993
- eISSN
- 1872-6240
- Language
- English
- Date published
- 2005
- Academic Unit
- Psychological and Brain Sciences; Neuroscience and Pharmacology; Health and Human Physiology
- Record Identifier
- 9984213405102771
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