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)

CRF1 and CRF2 receptors in the bed nucleus of the stria terminalis modulate the cardiovascular responses to acute restraint stress in rats

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)

Effect of lithium on behavioral disinhibition induced by electrolytic lesion of the median raphe nucleus

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Arterial pressure and gene expression in the nucleus of the solitary tract in rats fed with high-fat diet

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

Cardiovascular effects of chronically increasing angiotensin II type 2 receptor expression in the nucleus of the solitary tract

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

Distribution of melanin-concentrating hormone neurons projecting to the medial mammillary nucleus

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

Temporal changes in calcium-binding proteins in the medial geniculate nucleus of the monkey Sapajus apella

The subdivisions of the medial geniculate complex can be distinguished based on the immunostaining of calcium-binding proteins and by the properties of the neurons within each subdivision. The possibility of changes in neurochemistry in this and other central auditory areas are important aspects to understand the basis that contributing to functional variations determined by environmental cycles or the animal's cycles of activity and rest. This study investigated, for the first time, day/night differences in the amounts of parvalbumin-, calretinin- and calbindin-containing neurons in the thalamic auditory center of a non-human primate, Sapajus apella. The immunoreactivity of the PV-IR, CB-IR and CR-IR neurons demonstrated different distribution patterns among the subdivisions of the medial geniculate. Moreover, a high number of CB- and CR-IR neurons were found during day, whereas PV-IR was predominant at night. We conclude that in addition to the chemical heterogeneity of the medial geniculate nucleus with respect to the expression of calcium-binding proteins, expression also varied relative to periods of light and darkness, which may be important for a possible functional adaptation of central auditory areas to environmental changes and thus ensure the survival and development of several related functions.

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)

Unpredictable chronic mild stress exerts anxiogenic-like effects and activates neurons in the dorsal and caudal region and in the lateral wings of the dorsal raphe nucleus

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

Catecholaminergic neurons in the comissural region of the nucleus of the solitary tract modulate hyperosmolality-induced responses

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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.

Cardiovascular effects of the microinjection of L-proline into the third ventricle or the paraventricular nucleus of the hypothalamus in unanesthetized rats

We investigated the cardiovascular effects of the microinjection of L-proline (L-Pro) into the third ventricle (3V) and its peripheral mechanisms. Different doses of L-Pro into the 3V caused dose-related pressor and bradycardiac responses. The pressor response to L-Pro injected into the 3V was potentiated by intravenous pretreatment with the ganglion blocker pentolinium (5 mg/kg), thus excluding any significant involvement of the sympathetic nervous system. Because the response to the microinjection of L-Pro into the 3V was blocked by intravenous pretreatment with the V1-vasopressin receptor antagonist dTyr(CH2)5(Me)AVP (50 mu g/kg), it is suggested that these cardiovascular responses are mediated by a vasopressin release. The pressor response to the microinjection of L-Pro into the 3V was found to be mediated by circulating vasopressin, so, given that the paraventricular nucleus of the hypothalamus (PVN) is readily accessible from the 3V, we investigated whether the PVN could be a site of action for the L-Pro microinjected in the 3V. The microinjection of L-Pro (0.033 mu moles/0.1 mu l) into the PVN caused cardiovascular responses similar to those of injection of the 3V and were also shown to be mediated by vasopressin release. In conclusion, these results show that the microinjection of L-Pro into the 3V causes pressor and bradycardiac responses that could involve stimulation of the magnocellular cells of the PVN and release of vasopressin into the systemic circulation. Also, because the microinjection of L-Pro into the PVN caused a pressor response, this is the first evidence of cardiovascular effects caused by its injection in a supramedullary structure. (c) 2012 Wiley Periodicals, Inc.