GABAA receptor activation in the lateral parabrachial nucleus induces water and hypertonic NaCl intake

Callera, João Carlos; Oliveira, Lisandra Brandino de; Barbosa, Silas Pereira; Colombari, Débora S. A.; Luca, Laurival A. De; Menani, José Vanderlei

doi:10.1016/j.neuroscience.2005.05.009

Cited by 53 publications

(112 citation statements)

References 31 publications

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“…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%

“…The activation of GABA A , GABA B or opioid receptors with bilateral injections of muscimol, baclofen or ␤ endorphin, respectively, into the LPBN strongly increases 0.3 M NaCl intake by satiated or sodium depleted rats [20,27,29,30]. Therefore, the activation of GABA A , GABA B , opioid receptors in the LPBN deactivates the inhibitory mechanisms, releasing sodium intake if excitatory signals were activated by sodium depletion or not [20,27,29].…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, the activation of GABA A , GABA B , opioid receptors in the LPBN deactivates the inhibitory mechanisms, releasing sodium intake if excitatory signals were activated by sodium depletion or not [20,27,29].…”

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: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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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“…The doses of muscimol and bicuculline used in the present study were selected based on a previous study (22). The CeA injections were performed using a 10-μL Hamilton syringe connected by polyethylene tubing (PE-10) to an injector needle (0.3 mm OD).…”

Section: Drugsmentioning

confidence: 99%

GABA in the central amygdaloid nucleus modulates the electrolyte excretion and hormonal responses to blood volume expansion in rats

Margatho

Elias

2009

Braz J Med Biol Res

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We investigated the involvement of GABAergic mechanisms of the central amygdaloid nucleus (CeA) in unanesthetized rats subjected to acute isotonic or hypertonic blood volume expansion (BVE). Male Wistar rats bearing cannulas unilaterally implanted in the CeA were treated with vehicle, muscimol (0.2 nmol/0.2 μL) or bicuculline (1.6 nmol/0.2 μL) in the CeA, followed by isotonic or hypertonic BVE (0.15 or 0.3 M NaCl, 2 mL/100 g body weight over 1 min). The vehicle-treated group showed an increase in sodium excretion, urinary volume, plasma oxytocin (OT), and atrial natriuretic peptide (ANP) levels compared to control rats. Muscimol reduced the effects of BVE on sodium excretion (isotonic: 2.4 ± 0.3 vs vehicle: 4.8 ± 0.2 and hypertonic: 4.0 ± 0.7 vs vehicle: 8.7 ± 0.6 μEq·100 g -1 ·40 min -1 ); urinary volume after hypertonic BVE (83.8 ± 10 vs vehicle: 255.6 ± 16.5 μL·100 g -1 ·40 min -1 ); plasma OT levels (isotonic: 15.3 ± 0.6 vs vehicle: 19.3 ± 1 and hypertonic: 26.5 ± 2.6 vs vehicle: 48 ± 3 pg/ mL), and ANP levels (isotonic: 97 ± 12.8 vs vehicle: 258.3 ± 28.1 and hypertonic: 160 ± 14.6 vs vehicle: 318 ± 16.3 pg/mL). . .. . Bicuculline reduced the effects of isotonic or hypertonic BVE on urinary volume and ANP levels compared to vehicle-treated rats. However, bicuculline enhanced the effects of hypertonic BVE on plasma OT levels. These data suggest that CeA GABAergic mechanisms are involved in the control of ANP and OT secretion, as well as in sodium and water excretion in response to isotonic or hypertonic blood volume expansion.

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“…Sodium depletion stimulates the production of angiotensin II, which acts on the vascular organ of the lamina terminalis and the subfornical organ in the forebrain to stimulate salt intake. In the midbrain, the lateral parabrachial nucleus can powerfully inhibit sodium intake (1,2).…”

Section: Introductionmentioning

confidence: 99%

Changes in sodium appetite evoked by lesions of the commissural nucleus of the tractus solitarius

Ogihara

Schoorlemmer

Colombari

et al. 2009

Braz J Med Biol Res

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Ablation of the area postrema/caudal nucleus of the tractus solitarius (NTS) complex increases sodium intake, but the effect of selective lesions of the caudal NTS is not known. We measured depletion-induced sodium intake in rats with electrolytic lesions of the commissural NTS that spared the area postrema. One day after the lesion, rats were depleted of sodium with furosemide (10 mg/kg body weight, sc ) and then had access to water and a sodium-deficient diet for 24 h when 1.8% NaCl was offered. Water and saline intakes were measured for 2 h. Saline intake was higher in lesioned than in sham-lesioned rats (mean ± SEM: 20 ± 2 vs 11 ± 3 mL/2 h, P < 0.05, N = 6-7). Saline intake remained elevated in lesioned rats when the tests were repeated 6 and 14 days after the lesion, and water intake in these two tests was increased as well. Water intake seemed to be secondary to saline intake both in lesioned and in sham-lesioned rats. A second group of rats was offered 10% sucrose for 2 h/day before and 2, 7, and 15 days after lesion. Sucrose intake in lesioned rats was higher than in sham-lesioned rats only 7 days after lesioning. A possible explanation for the increased saline intake in rats with commissural NTS lesions could be a reduced gastrointestinal feedback inhibition. The commissural NTS is probably part of a pathway for inhibitory control of sodium intake that also involves the area postrema and the parabrachial nucleus.

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GABAA receptor activation in the lateral parabrachial nucleus induces water and hypertonic NaCl intake

Cited by 53 publications

References 31 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

GABA in the central amygdaloid nucleus modulates the electrolyte excretion and hormonal responses to blood volume expansion in rats

Changes in sodium appetite evoked by lesions of the commissural nucleus of the tractus solitarius

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