title: Role of 5-HT3 and 5-HT2C receptors located within the medial amygdala in the control of salt intake in sodium-depleted rats.
abstract: In the present study, we investigated the role of 5-HT(3) and 5-HT(2C) receptors located within the medial amygdala (MeA) in the control of water and salt intake in sodium-depleted rats. Pharmacological activation of 5-HT(3) receptors located in the medial amygdala by the selective 5-HT(3) receptor agonist m-CPBG significantly reduced salt intake in sodium-depleted rats, an effect that is reverted by pretreatment with the selective 5-HT(3) receptor antagonist ondansetron. In addition, the injection of ondansetron alone into the medial amygdala had no effect on salt intake in sodium-depleted and in sodium-repleted rats. Pharmacological stimulation of 5-HT(2C) receptors located in the medial amygdala by the selective 5-HT(2C) receptor agonist m-CPP failed to modify salt intake in sodium-depleted rats, whereas the blockade of these receptors by the selective 5-HT(2C) receptor antagonist SDZ SER 082 significantly reduced salt intake in this same group of animals. These results lead to the conclusion that the pharmacological activation of 5-HT(3) receptors located within the MeA inhibits salt intake in sodium-depleted rats and that, in this same brain region, the functional integrity of 5-HT(2C) receptors is required to achieve the full expression of sodium appetite in sodium-depleted rats.
authors.affiliation: Department of Biological Sciences, State University of Southwest Bahia, Jequié, Brazil.
authors.forename: Carla
authors.initials: C
authors.lastname: Luz
authors.forename: Anderson
authors.initials: A
authors.lastname: Souza
authors.forename: Rodolfo
authors.initials: R
authors.lastname: Reis
authors.forename: Josmara Bartolomei
authors.initials: JB
authors.lastname: Fregoneze
authors.forename: Emilio
authors.initials: E
authors.lastname: de Castro e Silva
mesh_terms: D000679:Amygdala / Q000187:drug effects / Q000378:metabolism*; D000704:Analysis of Variance; D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects / Q000502:physiology; D001522:Behavior, Animal; D001645:Biguanides / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004326:Drinking / Q000187:drug effects; D004347:Drug Interactions; D005247:Feeding Behavior / Q000187:drug effects / Q000502:physiology*; D005665:Furosemide / Q000633:toxicity; D008297:Male; D017294:Ondansetron / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D044405:Receptor, Serotonin, 5-HT2C / Q000502:physiology*; D044406:Receptors, Serotonin, 5-HT3 / Q000502:physiology*; D051437:Renal Insufficiency / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology; D012439:Saccharin / Q000378:metabolism; D012702:Serotonin Antagonists / Q000494:pharmacology; D017366:Serotonin Receptor Agonists / Q000494:pharmacology; D012964:Sodium / Q000172:deficiency / Q000378:metabolism*; D013997:Time Factors
chemical_list: D001645:Biguanides; D044405:Receptor, Serotonin, 5-HT2C; D044406:Receptors, Serotonin, 5-HT3; D012702:Serotonin Antagonists; D017366:Serotonin Receptor Agonists; D017294:Ondansetron; D005665:Furosemide; C065734:1-(3-chlorophenyl)biguanide; D012964:Sodium; D012439:Saccharin