Role of the lateral parabrachial nucleus in the control of sodium appetite

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

ANGIOTENSINERGIC AND CHOLINERGIC RECEPTORS OF THE SUBFORNICAL ORGAN MEDIATE SODIUM INTAKE INDUCED BY GABAergic ACTIVATION OF THE LATERAL PARABRACHIAL NUCLEUS

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Gabaergic and opioid receptors mediate the facilitation of NaCl intake induced by α₂-adrenergic activation in the lateral parabrachial nucleus

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Moxonidine into the lateral parabrachial nucleus modifies postingestive signals involved in sodium intake control

The activation of a2-adrenoceptors with bilateral injections of moxonidine (a2-adrenoceptor and imidazoline receptor agonist) into the lateral parabrachial nucleus (LPBN) increases 1.8% NaCl intake induced by treatment with furosemide (FURO) + captopril (CAP) subcutaneously. In the present study, we analyzed licking microstructure during water and 1.8% NaCl intake to investigate the changes in orosensory and postingestive signals produced by moxonidine injected into the LPBN. Male Sprague–Dawley rats were treated with FURO + CAP combined with bilateral injections of vehicle or moxonidine (0.5 nmol/0.2 ll) into the LPBN. Bilateral injections of moxonidine into the LPBN increased FURO + CAP-induced 1.8% NaCl intake, without changing water intake. Microstructural analysis of licking behavior found that this increase in NaCl intake was a function of increased number of licking bursts from 15 to 75 min of the test (maximum of 49 ± 9 bursts/bin, vs. vehicle: 2 ± 2 bursts/bin). Analysis of the first 15 min of the test, when most of the licking behavior occurred, found no effect of moxonidine on the number of licks/burst for sodium intake (24 ± 5 licks/burst, vs. vehicle: 27 ± 8 licks/burst). This finding suggests that activation of a2-adrenoceptors in the LPBN affects postingestive signals that are important to inhibit and limit sodium intake by FURO + CAP-treated rats.

Sodium intake combining cholinergic activation and noradrenaline into the lateral parabrachial nucleus

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Gabaergic and opioid receptors mediate the facilitation of NaCl intake induced by alpha(2)-adrenergic activation in the lateral parabrachial nucleus

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Importance of the central nucleus of the amygdala on sodium intake caused by deactivation of lateral parabrachial nucleus

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Sodium intake, brain c-Fos protein and gastric emptying in cell-dehydrated rats treated with methysergide into the lateral parabrachial nucleus

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Role of alfa2-adrenoceptors in the lateral parabrachial nucleus in the control of body fluid homeostasis

Central α2-adrenoceptors and the pontine lateral parabrachial nucleus (LPBN) are involved in the control of sodium and water intake. Bilateral injections of moxonidine (α2-adrenergic/imidazoline receptor agonist) or noradrenaline into the LPBN strongly increases 0.3 M NaCl intake induced by a combined treatment of furosemide plus captopril. Injection of moxonidine into the LPBN also increases hypertonic NaCl and water intake and reduces oxytocin secretion, urinary sodium, and water excreted by cell-dehydrated rats, causing a positive sodium and water balance, which suggests that moxonidine injected into the LPBN deactivates mechanisms that restrain body fluid volume expansion. Pretreatment with specific α2-adrenoceptor antagonists injected into the LPBN abolishes the behavioral and renal effects of moxonidine or noradrenaline injected into the same area, suggesting that these effects depend on activation of LPBN α2-adrenoceptors. In fluid-depleted rats, the palatability of sodium is reduced by ingestion of hypertonic NaCl, limiting intake. However, in rats treated with moxonidine injected into the LPBN, the NaCl palatability remains high, even after ingestion of significant amounts of 0.3 M NaCl. The changes in behavioral and renal responses produced by activation of α2-adrenoceptors in the LPBN are probably a consequence of reduction of oxytocin secretion and blockade of inhibitory signals that affect sodium palatability. In this review, a model is proposed to show how activation of α2-adrenoceptors in the LPBN may affect palatability and, consequently, ingestion of sodium as well as renal sodium excretion.

Lesions of the commissural subnucleus of the nucleus of the solitary tract increase isoproterenol-induced water intake

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LATERAL PARABRACHIAL SEROTONERGIC MECHANISMS - ANGIOTENSIN-INDUCED PRESSOR AND DRINKING RESPONSES

This study investigated the effects of bilateral injections of serotonergic receptor ligands into the lateral parabrachial nucleus (LPBN) on the presser and dipsogenic responses induced by intracerebroventricular (icv) injection of angiotensin II (ANG II). Rats with stainless steel cannulas implanted bilaterally into the LPBN and into the left lateral ventricle were used to study icy ANG II-induced water intake and presser responses. Pretreatment with the serotonergic 5-HT1/5-HT2 receptor antagonist methysergide (1-8 mu g/200 nl) bilaterally injected into the LPBN increased the water intake induced by icv ANG II (50 ng/mu l) administered via the lateral ventricle, but pretreatment with methysergide (4 mu g/200 nl) did not change the presser response produced by icy ANG II. After bilateral injection of either serotonin (5-HT, 5 mu g/200 nl) or the serotonergic 5-HT2a/5-HT2c receptor agonist (+/-)-2,5-dimetoxy-4-iodoamphetamine hydrochloride (DOI; 0.5-10 mu g/200 nl) into the LPBN, the water intake induced by ANG II was significantly reduced. These results are consistent with other observations indicating that the LPBN is associated with inhibitory mechanisms controlling water intake induced by ANG II treatment and suggest that serotonergic pathways may be involved in this effect.

Forebrain angiotensin type 1 receptors and parabrachial serotonin in the control of NaCl and water intake

This study investigated the roles of serotonin (5-HT) receptors in the lateral parabrachial nucleus (LPBN), and brain angiotensin type 1 (AT(1)) receptors in the intake of 0.3 M NaCl and water induced by angiotensin II (ANG II). Rats were implanted with stainless steel cannulas for injections into tho subfornical organ (SFO) and into the LPBN. Bilateral LPBN pretreatment with the nonselective serotonergic 5-HT1/5-HT2 receptor antagonist methysergide (4 mu g/200 nl) markedly enhanced 0.3 M NaCl intake induced by injections of ANG II (20 ng/200 nl) into the SFO. Pretreatment of the SFO with the AT(1) receptor antagonist losartan (1 mu g/200 nl) blocked the intake of 0.3 M NaCl induced by ANG II in combination with LPBN methysergide injections. These results suggest that serotonergic mechanisms associated with the LPBN inhibit the expression of salt appetite induced by ANG II injections into Ihs SFO. In addition, the results indicate that the enhanced NaCl intake generated by central administration of ANG II in the presence of LPBN 5-HT blockade is mediated bg brain ATI receptors.

Brain serotonin blockade and paradoxical salt intake in rats

Serotonin antagonism in the lateral parabrachial nucleus (LPBN) enhances sodium appetite induced by hypovolaemia and angiotensin-mineralocorticoid activation, but produces no sodium intake in euhydrated animals. In the present work, male adult rats (n=21) that received bilateral injections of the serotonergic antagonist methysergide (4 mug/ 0.2 mul) into the LPBN combined to intragastric load of 2 M NaCl (2 ml/rat), ingested hypertonic NaCl (ingestion of 4.3+/-1.6 ml/2 h of 0.3 M NaCl versus vehicle into LPBN: 0.2+/-0.2 ml/2 h, P<0.05). Methysergide- and vehicle-treated animals also ingested water (9.5+/-0.7 and 7.2+/-0.5 ml/2 h, respectively, P>0.05) as expected from the state of cell dehydration produced by the load. Ingestion of water (11.0+/-1.2 ml/2 h), and of 0.3 M NaCl (1.1+/-0.7 ml/2 h) were not altered by methysergide in NaCl loaded rats with misplaced LPBN injections (n=15). The ingestion of hypertonic NaCl by rats with serotonergic blockade in the LPBN suggests that the circuits subserving sodium appetite are activated, but at the same time strongly inhibited through the LPBN, during cell dehydration. (C) 2003 IBRO. Published by Elsevier Ltd. All rights reserved.

Water deprivation and the double- depletion hypothesis: common neural mechanisms underlie thirst and salt appetite

Water deprivation-induced thirst is explained by the double-depletion hypothesis, which predicts that dehydration of the two major body fluid compartments, the extracellular and intracellular compartments, activates signals that combine centrally to induce water intake. However, sodium appetite is also elicited by water deprivation. In this brief review, we stress the importance of the water-depletion and partial extracellular fluid-repletion protocol which permits the distinction between sodium appetite and thirst. Consistent enhancement or a de novo production of sodium intake induced by deactivation of inhibitory nuclei (e.g., lateral parabrachial nucleus) or hormones (oxytocin, atrial natriuretic peptide), in water-deprived, extracellular-dehydrated or, contrary to tradition, intracellular-dehydrated rats, suggests that sodium appetite and thirst share more mechanisms than previously thought. Water deprivation has physiological and health effects in humans that might be related to the salt craving shown by our species.