Abstract

The present study determined the effect of an electrolytic lesion of the dorsal raphe nucleus (DRN) on water intake and sodium appetite. Male Wistar rats weighing 290-320 g with a lesion of the DRN (L-DRN), performed two days before experiments and confirmed by histology at the end of the experiments, presented increased sensitivity to the dehydration induced by fluid deprivation. The cumulative water intake of L-DRN rats reached 23.3 1.9 ml (a 79% increase, N = 9) while sham-lesioned rats (SL-DRN) did not exceed 13.0 1.0 ml (N = 11, P < 0.0001) after 5 h. The L-DRN rats treated with isoproterenol (300 g kg-1 ml-1, sc) exhibited an increase in water intake that persisted throughout the experimental period (L-DRN, 15.7 1.47 ml, N = 9 vs SL-DRN, 9.3 1.8 ml, N = 11, P < 0.05). The L-DRN rats also showed an increased spontaneous sodium appetite during the entire period of assessment. The intake of 0.3 M NaCl after 12, 24, 36 and 72 h by the L-DRN rats was always higher than 20.2 4.45 ml (N = 10), while the intake by SL-DRN was always lower than 2.45 0.86 ml (N = 10, P < 0.00001). Sodium- and water-depleted L-DRN rats also exhibited an increased sodium appetite (13.9 2.0 ml, N = 11) compared to SL-DRN (4.6 0.64 ml, N = 11) after 120 min of observation (P < 0.02). The sodium preference of L-DRN rats in both conditions was always higher than that of SL-DRN rats. These results suggest that electrolytic lesion of the DRN overcomes a tonic inhibitory component of sodium appetite.

Highlights

  • Serotonergic neurons of the mesencephalic dorsal raphe nucleus (DRN), located in its medial portion, project to prosencephalic regions involved in hydroelectrolytic and cardiocirculatory homeostasis [1,2,3,4]

  • The results of the present study reveal that electrolytic lesions of the DRN produced an increase in sensitivity to osmotic stimulation by dehydration induced by fluid deprivation and ß-adrenergic stimulation with isoproterenol

  • This observation is consistent with the hypothesis that neurons of the DRN, which are probably serotonergic, exert a modulatory influence on the thirst related to an increase in the tonicity of extracellular fluid or on the thirst signaled by increased plasma levels of angiotensin II- (ANG II) [4,19,20,21]

Read more

Summary

Introduction

Serotonergic neurons of the mesencephalic dorsal raphe nucleus (DRN), located in its medial portion, project to prosencephalic regions involved in hydroelectrolytic and cardiocirculatory homeostasis [1,2,3,4]. The short and long term, the changes in volume, pressure and sodium concentration in the extracellular fluid, evokes electrophysiological changes in the DRN [7] In this context, it has been shown that the microinjection of serotonergic agonists of the 5HT2A and 5HT2C receptors into the SFO excites angiotensin II- (ANG II) sensitive neurons [8]. Relevant observations have shown that stimulation of the AV3V region by intracerebroventricular (icv) administration of serotonin, serotonin-releasing agents or 5HT2A/2C agonists increases the urinary excretion of sodium [12,13] All of these stimulation conditions under fluid deprivation, cholinergic or angiotensinergic stimulation of the AV3V region and central or systemic ßadrenergic stimulation caused a decrease in water intake [14,15,16]. Spontaneous sodium appetite was investigated in DRN-lesioned rats following a simultaneous offer of water and hypertonic saline for three consecutive days

Material and Methods
Experimental procedures
Results
Discussion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.