1. Dipsogenic stimulation in ibotenic DRN-lesioned rats induces concomitant sodium appetite.
- Author
-
Cavalcante-Lima HR, Lima HR, Costa-e-Sousa RH, Olivares EL, Cedraz-Mercez PL, Reis RO, Badauê-Passos D Jr, De-Lucca W Jr, de Medeiros MA, Côrtes Wda S, and Reis LC
- Subjects
- Animals, Appetite drug effects, Drinking drug effects, Drinking physiology, Male, Neurotoxins toxicity, Rats, Rats, Wistar, Appetite physiology, Ibotenic Acid toxicity, Raphe Nuclei drug effects, Raphe Nuclei physiology, Sodium administration & dosage, Sodium, Dietary analysis, Thirst drug effects, Thirst physiology
- Abstract
The main purpose of this study was to investigate whether dipsogenic stimuli influences the sodium appetite of rats with ibotenic acid lesion of the dorsal raphe nucleus (IBO-DRN). Compared to control, rats microinjected with phosphate buffer (PB-DRN), the ingestion of 0.3M NaCl was enhanced in IBO-DRN at 21 and 35 days after DRN lesion under a protocol of fluids and food deprivation. Despite of similar dipsogenic response observed both in IBO-DRN and PB-DRN treated with isoproterenol (ISO, 300 microg/kg, sc), the 0.3M NaCl intake was again significantly enhanced in IBO-DRN at 21 and 35 days post-lesion. Finally, treatment with polyethylene glycol (PEG, MW=20,000, 20%, w/v, 16.7 ml/kg, sc) induced higher dipsogenic response in IBO-DRN than PB-DRN at 21 day after lesion. In addition, IBO-DRN also expressed higher sodium appetite than PB-DRN, concomitantly with a drinking response. These results suggest that ibotenic lesion of DRN promote an increase of the brain angiotensinergic response, possibly settled within the subfornical organ, through paradigms which increase circulating ANG II levels. The current paper supports the hypothesis that the ibotenic lesion of DRN suppresses a serotonergic component implicated on the modulation of the sodium appetite and, therefore, furthering homeostatic restoration of extracellular fluid volume.
- Published
- 2005
- Full Text
- View/download PDF