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

Gasparini, Silvia; Andrade-Franzé, G.M.F.; Gomide, Joelma Maria Cardoso; Andrade, C.A.F.; Luca, Laurival A. De; Colombari, Débora S. A.; Paula, Patrícia Maria de; Menani, José Vanderlei

doi:10.1016/j.neuroscience.2015.04.059

Cited by 3 publications

(2 citation statements)

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“…These signals may modulate the activity of LPBN inhibitory mechanisms by releasing different neurotransmitters like serotonin, cholecystokinin, corticotrophin-releasing factor (CRF) and glutamate which increase the inhibitory action, whereas others like GABA, opioids, ATP and noradrenaline reduce the inhibitory action (Andrade et al, 2004Callera et al, 2005;De Gobbi et al, 2009, Gasparini et al, 2009, De Oliveira et al, 2007, 2008Menezes et al, 2011Menezes et al, , 2014Roncari et al, 2014). The deactivation of the inhibitory mechanisms by changing the activity of specific neurotransmitters/receptors in the LPBN increases hypertonic NaCl and/ or water intake induced by different dipsogenic or natriorexigenic stimuli like angiotensin II (ANG II), sodium depletion, water deprivation, central cholinergic activation or even osmoreceptor activation Johnson, 1995, 1998;Menani et al, 1996Menani et al, , 2002Menani et al, , 2014De Luca et al, 2003;Andrade et al, 2004Andrade et al, , 2006De Gobbi et al, 2009;Gasparini et al, 2015b). In addition, the neuronal deactivation with bilateral injection of the GABA A agonist muscimol into the LPBN stimulates hypertonic NaCl intake by euhydrated rats (Callera et al, 2005;De Oliveira et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2015

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The lateral parabrachial nucleus (LPBN) and the central nucleus of the amygdala (CeA) are important central areas for the control of sodium appetite. In the present study, we investigated the importance of the facilitatory mechanisms of the CeA on NaCl and water intake produced by the deactivation of LPBN inhibitory mechanisms. Male Holtzman rats (n=7-14) with stainless steel cannulas implanted bilaterally in the CeA and LPBN were used. Bilateral injections of moxonidine (α2-adrenoceptor/imidazoline agonist, 0.5 nmol/0.2 μl) into the LPBN increased furosemide+captopril-induced 0.3M NaCl (29.7 ± 7.2, vs. vehicle: 4.4 ± 1.6 ml/2h) and water intake (26.4 ± 6.7, vs. vehicle: 8.2 ± 1.6 ml/2h). The GABAA agonist muscimol (0.25 nmol/0.2 μl) injected bilaterally into the CeA abolished the effects of moxonidine into the LPBN on 0.3M NaCl (2.8 ± 1.6 ml/2h) and water intake (3.3 ± 2.3 ml/2h). Euhydrated rats treated with muscimol (0.5 nmol/0.2 μl) into the LPBN also ingested 0.3M NaCl (19.1 ± 6.4 ml/4h) and water (8.8 ± 3.2 ml/4h). Muscimol (0.5 nmol/0.2 μl) into the CeA also abolished 0.3M NaCl (0.1 ± 0.04 ml/4h) and water intake (0.1 ± 0.02 ml/4h) in euhydrated treated with muscimol into the LPBN. The present results show that neuronal deactivation of the CeA abolishes NaCl intake produced by the blockade of LPBN inhibitory mechanisms, suggesting an interaction between facilitatory mechanisms of the CeA and inhibitory mechanisms of the LPBN in the control of NaCl intake.

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Section: Introductionmentioning

confidence: 99%

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

et al. 2015

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“…The activation of α 2 -adrenoceptors with bilateral injections of noradrenaline or the α 2 -adrenoceptor agonist moxonidine into the LPBN increases 0.3 M NaCl intake induced by dipsogenic or natriorexigenic stimuli (Andrade et al, 2004;Andrade et al, 2006Andrade et al, , 2007Andrade et al, 2015;Gasparini et al, 2015a;Gasparini et al, 2015b). In addition to increase fluid depletion-induced sodium intake, the activation of GABA or opioid receptors in the LPBN also induces strong ingestion of hypertonic NaCl and water in normohydrated rats (Callera et al, 2005b;de Oliveira et al, 2007;De Oliveira et al, 2008;De Oliveira et al, 2011), suggesting an important role of the LPBN inhibitory mechanisms limiting or restraining sodium intake in different conditions and even in normohydrated animals.…”

Section: Introductionmentioning

confidence: 99%

Opioid and α2 adrenergic mechanisms are activated by GABA agonists in the lateral parabrachial nucleus to induce sodium intake

Oliveira

Andrade

Luca

et al. 2018

Brain Research Bulletin

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The activation of GABA, opioid or α adrenergic mechanisms in the lateral parabrachial nucleus (LPBN) facilitates hypertonic NaCl intake in rats. In the present study, we combined opioid or α adrenergic antagonists with GABA agonists into the LPBN in order to investigate if NaCl intake caused by GABAergic activation in normohydrated rats depends on opioid or α-adrenergic mechanisms in this area. Male Holtzman rats with stainless steel cannulas implanted bilaterally in the LPBN were used. Bilateral injections of muscimol or baclofen (GABA and GABA agonists, respectively, 0.5 nmol/0.2 μl) into the LPBN induced strong ingestion of 0.3 M NaCl (45.8 ± 7.3 and 21.8 ± 4.8 ml/240 min, respectively) and water intake (22.7 ± 3.4 and 6.6 ± 2.5 ml/240 min, respectively). Naloxone (opioid antagonist, 150 nmol/0.2 μl) into the LPBN abolished 0.3 M NaCl and water intake to muscimol (2.0 ± 0.6 and 0.9 ± 0.2 ml/240 min, respectively) or baclofen (2.3 ± 1.1 and 0.8 ± 0.4 ml/240 min, respectively). RX 821002 (α adrenoceptor antagonist, 10 nmol/0.2 μl) into the LPBN reduced 0.3 M NaCl intake induced by the injections of muscimol or baclofen (26.6 ± 8.0 and 10.1 ± 4.9 ml/240 min, respectively). RX 821002 reduced water intake induced by muscimol (7.7 ± 2.9 ml/240 min), not by baclofen. The results suggest that sodium intake caused by gabaergic activation in the LPBN in normohydrated rats is totally dependent on the activation of opioid mechanisms and partially dependent on the activation of α adrenergic mechanisms in the LPBN.

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Central muscarinic and LPBN mechanisms on sodium intake

Anesio

Barbosa

Luca

et al. 2019

Brain Research Bulletin

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

Cited by 3 publications

References 38 publications

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

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

Opioid and α2 adrenergic mechanisms are activated by GABA agonists in the lateral parabrachial nucleus to induce sodium intake

Central muscarinic and LPBN mechanisms on sodium intake

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