Effect of electrolytic lesion of the dorsal raphe nucleus on water intake and sodium appetite

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 µg 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. Correspondence

Chronic excitotoxic lesion of the dorsal raphe nucleus induces sodium appetite

“…Taken together, this evidence supports our view that central control of sodium satiety and excretion is regulated by the serotonergic system that originates from the midbrain, but only one study acknowledged that the suppression of ascending serotonergic pathways through DRN electrolytic lesion evokes an increase in sodium appetite (21). Corroborating these findings, other investigators showed that basal c-Fos expression in serotonergic neurons of the DRN decreased after sodium depletion induced by peritoneal dialysis and increased after spontaneous and induced sodium intake, suggesting that there is a tonic inhibition of sodium appetite by serotonergic cells of this nucleus (11).…”

“…Corroborating these findings, other investigators showed that basal c-Fos expression in serotonergic neurons of the DRN decreased after sodium depletion induced by peritoneal dialysis and increased after spontaneous and induced sodium intake, suggesting that there is a tonic inhibition of sodium appetite by serotonergic cells of this nucleus (11). Although we hypothesized the same, when working with DRN electrolytic lesion it is necessary to limit the lesion to the neuronal cell body located in the ventromedial portion of the DRN and to perform longer observations (21).…”

“…It has been postulated that the DRN serotonergic neurons receive viscerosensory inputs concerning renal sodium load and/or ECF volume variations to trigger homeostatic regulation of sodium appetite (6,21,30). This view has not shown).…”

“…DRN afferent fibers arise from these areas (especially the SFO), probably involved in a feedback loop regulating sodium satiety and contributing to ECF volume and cardiocirculatory homeostasis (7,9,21).…”

Effect of L-5-Hydroxytryptophan on drinking behavior in Coturnix japonica (Temminck and Schlegel, 1849) (Galliformes: Aves): involvement of renin-angiotensin system

“…Behavior, such as drinking and feeding are constantly monitored by 5-HT-containing neurons in mammals and birds. Studies in our laboratory evidenced the serotonergic neurons influence in the sodium appetite and food and water intake behavior (Badauê-Passos Jr et al, 2003;Olivares et al, 2003;Lima et al, 2004;Cavalcante-Lima et al, 2005a,b;Cedraz-Mercez et al, 2005;Medeiros et al, 2005). In rats, peripheral administration of either 5-HT or its precursor 5-HTP induces water intake via renal renin-angiotensin system (RAS) activation (Rowland et al, 1987), however they display opposed effects when centrally applied.…”