Activation of α2-adrenergic receptors into the lateral parabrachial nucleus enhances NaCl intake in rats

Andrade, C.A.F.; Barbosa, Silas Pereira; Luca, Laurival A. De; Menani, José Vanderlei

doi:10.1016/j.neuroscience.2004.07.042

Cited by 47 publications

(90 citation statements)

References 34 publications

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“…Injections centered in the ventral lateral and external lateral portions, as well as in the Kölliker-Fuse nucleus observed in some rats were also considered as correctly placed in the LPBN. The sites of the injections in the present study were similar to those of previous studies that showed the effects of moxonidine, muscimol or opioids injected into the LPBN on NaCl and water intake [19][20][21]24,27].…”

Section: Discussionsupporting

confidence: 86%

“…Bicuculline and naloxone abolish 0.3 M NaCl and water intake induced respectively by muscimol and ␤-endorphin injected into the LPBN of satiated, fluid replete, rats [20,27,29]. Moxonidine, however, has no effect on sodium or water intake when injected into the LPBN of satiated rats [21]. It has been hypothesized that the threshold to increase hypertonic sodium intake when GABA and opioid neurotransmission are activated is much lower than that required to increase NaCl intake when, for example, ␣ 2 -adrenoceptors are activated [34].…”

Section: Discussionmentioning

confidence: 95%

“…The activation of the ␣ 2 -adrenoceptors with bilateral injections of noradrenaline or moxonidine into the LPBN increases 0.3 M NaCl and water intake induced by the treatment with the diuretic furosemide (FURO) combined with low dose of the angiotensin converting enzyme inhibitor captopril (CAP) injected subcutaneously. Activation of the same receptors in the LPBN has no effect on water and hypertonic NaCl intake of satiated rats [21,25].…”

Section: Introductionmentioning

confidence: 92%

“…Water, 0.3 M NaCl and food were removed and the animals received subcutaneous FURO (10 mg/kg of body wt) + CAP (5 mg/kg of body wt) as described previously [7,21,31]. One hour later, water and 0.3 M NaCl were provided in burettes with 0.1-ml divisions that were fitted with metal drinking spouts.…”

Section: Ingestive Testmentioning

confidence: 99%

“…Studies that have investigated the involvement of the LPBN in the control of fluid-electrolyte balance demonstrated that different neurotransmitters like serotonin, cholecystokinin, glutamate and corticotrophin releasing factor (CRF) or receptors like ␣ 2 -adrenoceptors, GABAergic, opioid or purinergic receptors in the LPBN are involved with the control of sodium intake [1,3,5,[18][19][20][21][22][23][24][25][26][27][28]. The activation of the ␣ 2 -adrenoceptors with bilateral injections of noradrenaline or moxonidine into the LPBN increases 0.3 M NaCl and water intake induced by the treatment with the diuretic furosemide (FURO) combined with low dose of the angiotensin converting enzyme inhibitor captopril (CAP) injected subcutaneously.…”

Section: Introductionmentioning

confidence: 99%

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

Andrade

Oliveira

Andrade-Franzé

et al. 2015

Behavioural Brain Research

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Alpha2-adrenergic, gabaergic or opioidergic activation in the lateral parabrachial nucleus (LPBN) increases sodium intake. In the present study, we investigated the effects of single or combined blockade of opioidergic and gabaergic receptors in the LPBN on the increase of 0.3M NaCl intake induced by α2-adrenoceptor activation in the LPBN. Male Holtzman rats (n=5-9/group) with cannulas implanted bilaterally in the LPBN were treated with the diuretic furosemide (10 mg/kg b wt.) combined with low dose of the angiotensin converting enzyme inhibitor captopril (5 mg/kg b wt.) subcutaneously. Bilateral injections of moxonidine (alpha2-adrenergic/imidazoline receptor agonist, 0.5 nmol) into the LPBN increased furosemide+captopril-induced 0.3M NaCl intake (25.8±1.4, vs. vehicle: 3.8±1.1 ml/60 min). The opioidergic receptor antagonist naloxone (100 nmol) or the GABAA receptor antagonist bicuculline (5 nmol) injected into the LPBN partially reduced the increase of 0.3M NaCl intake produced by LPBN moxonidine (11.8±4.0 and 22.8±4.5, respectively, vs. vehicle+moxonidine: 31.6±4.0 ml/60 min, respectively). Similar to the treatment with each antagonist alone, the combined injections of naloxone (100 nmol) and bicuculline (5 nmol) into the LPBN also partially reduced moxonidine effects on 0.3M NaCl intake (15.5±6.5 ml/60 min). The GABAB receptor antagonist saclofen (5 nmol) injected into the LPBN did not change the effects of moxonidine on 0.3M NaCl intake (24.3±7.8 ml/120 min). These results suggest that the increase of 0.3M NaCl intake by α2-adrenergic receptor activation in the LPBN is partially dependent on GABAA and opioid receptor activation in this area.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 92%

Section: Ingestive Testmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

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

Andrade

Oliveira

Andrade-Franzé

et al. 2015

Behavioural Brain Research

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Sodium deprivation and salt intake activate separate neuronal subpopulations in the nucleus of the solitary tract and the parabrachial complex

Geerling

Loewy

2007

J of Comparative Neurology

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Salt intake is an established response to sodium deficiency, but the brain circuits that regulate this behavior remain poorly understood. We studied the activation of neurons in the nucleus of the solitary tract (NTS) and their efferent target nuclei in the pontine parabrachial complex (PB) in rats during sodium deprivation and after salt intake. After 8-day dietary sodium deprivation, immunoreactivity for c-Fos (a neuronal activity marker) increased markedly within the aldosterone-sensitive neurons of the NTS, which express the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2). In the PB, c-Fos labeling increased specifically within two sites that relay signals from the HSD2 neurons to the forebrain--the pre-locus coeruleus and the innermost region of the external lateral parabrachial nucleus. Then, 1-2 hours after sodium-deprived rats ingested salt (a hypertonic 3% solution of NaCl), c-Fos immunoreactivity within the HSD2 neurons was virtually eliminated, despite a large increase in c-Fos activation in the surrounding NTS (including the A2 noradrenergic neurons) and area postrema. Also after salt intake, c-Fos activation increased within pontine nuclei that relay gustatory (caudal medial PB) and viscerosensory (rostral lateral PB) information from the NTS to the forebrain. Thus, sodium deficiency and salt intake stimulate separate subpopulations of neurons in the NTS, which then transmit this information to the forebrain via largely separate relay nuclei in the PB complex. These findings offer new perspectives on the roles of sensory information from the brainstem in the regulation of sodium appetite.

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The Neuroendocrinology, Neurochemistry and Molecular Biology of Thirst and Salt Appetite

Johnson¹,

Thunhorst²

2007

Handbook of Neurochemistry and Molecular Neurobiology

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Activation of α2-adrenergic receptors into the lateral parabrachial nucleus enhances NaCl intake in rats

Cited by 47 publications

References 34 publications

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

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

Sodium deprivation and salt intake activate separate neuronal subpopulations in the nucleus of the solitary tract and the parabrachial complex

The Neuroendocrinology, Neurochemistry and Molecular Biology of Thirst and Salt Appetite

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