The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
José Vanderlei Menani - One of the best experts on this subject based on the ideXlab platform.
-
Mineral preference in rats treated with muscimol into the Lateral Parabrachial Nucleus
Neuroscience letters, 2020Co-Authors: João Carlos Callera, Laurival A De Luca, José Vanderlei MenaniAbstract:Abstract Injection of muscimol, a GABAA receptor agonist, into the Lateral Parabrachial Nucleus (LPBN) induces 0.3 M NaCl intake in rats. In the present work, we investigated whether such an effect applies to hypertonic (0.3 M) mineral solutions in general or is selective to sodium solutions in a 240 min intake test. Muscimol injection (0.5 nmol/0.2 μL) compared to vehicle injection into the LPBN of adult hydrated rats produced a preferential ingestion of 0.3 M NaCl (25.3 ± 10.2 mL) followed by a 0.3 M NaHCO3 intake (11.7 ± 5.6 mL), with no significant effect on water, KCl and CaCl2 intake. Only the effect of muscimol on NaCl intake (19.0 ± 10.4 mL) persisted in cell-dehydrated rats, with hardly any effect on water or other mineral solutions. The results suggest that the LPBN controls the ingestion of hypertonic NaCl and NaHCO3. They also suggest a selective mechanisms involving the LPBN to check hypertonic sodium intake.
-
Opioid and α2 adrenergic mechanisms are activated by GABA agonists in the Lateral Parabrachial Nucleus to induce sodium intake.
Brain Research Bulletin, 2018Co-Authors: Lisandra Brandino De Oliveira, Laurival A De Luca, Carina Aparecida Fabrício De ,andrade, Debora S. A. Colombari, José Vanderlei MenaniAbstract:Abstract The activation of GABA, opioid or α2 adrenergic mechanisms in the Lateral Parabrachial Nucleus (LPBN) facilitates hypertonic NaCl intake in rats. In the present study, we combined opioid or α2 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 α2-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 (GABAA and GABAB 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 (α2 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 α2 adrenergic mechanisms in the LPBN.
-
the Lateral Parabrachial Nucleus and central angiotensinergic mechanisms in the control of sodium intake induced by different stimuli
Behavioural Brain Research, 2017Co-Authors: Camila F Roncari, Laurival A De Luca, Debora S. A. Colombari, Patricia M De Paula, Eduardo Colombari, R B David, José Vanderlei MenaniAbstract:Abstract Angiotensin II (ANG II) is a typical facilitatory stimulus for sodium appetite. Surprisingly, hyperosmolarity and central cholinergic stimulation, two classical antinatriorexigenic stimuli, also facilitate NaCl intake when they are combined with injections of the α 2 -adrenoceptor/imidazoline agonist moxonidine into the Lateral Parabrachial Nucleus (LPBN). In the present study, we tested the relative importance of central angiotensinergic and cholinergic mechanisms for the control of water and NaCl intake by combining different dipsogenic or natriorexigenic stimuli with moxonidine injection into the LPBN. Adult male Holtzman rats (n = 9–10/group) with stainless steel cannulas implanted in the Lateral ventricle and LPBN were used. BiLateral injections of moxonidine (0.5 nmol) into the LPBN increased water and 0.3 M NaCl intake in rats that received furosemide + captopril injected subcutaneously, ANG II (50 ng) or carbachol (cholinergic agonist, 4 nmol) injected intracerebroventricularly (icv) or 2 M NaCl infused intragastrically (2 ml/rat). Losartan (AT 1 antagonist, 100 μg) or atropine (muscarinic antagonist, 20 nmol) injected icv abolished the effects on water and 0.3 M NaCl of moxonidine combined to either 2 M NaCl intragastrically or carbachol icv. However, atropine icv did not change 0.3 M NaCl intake produced by direct central action of ANG II like that induced by ANG II icv or furosemide + captopril combined with moxonidine into the LPBN. The results suggest that different stimuli, including hyperosmolarity and central cholinergic stimulation, share central angiotensinergic activation as a common mechanism to facilitate sodium intake, particularly when they are combined with deactivation of the LPBN inhibitory mechanisms.
-
rapid stimulation of sodium intake combining aldosterone into the 4th ventricle and the blockade of the Lateral Parabrachial Nucleus
Neuroscience, 2017Co-Authors: Silvia Gasparini, José Vanderlei Menani, G M F Andradefranze, Mariana Rosso Melo, G F Leite, P A Nascimento, Eduardo ColombariAbstract:Chronic infusion of aldosterone into the 4th ventricle (4th V) induces robust daily sodium intake, whereas acute injection of aldosterone into the 4th V produces no sodium intake. The inhibitory mechanism of the Lateral Parabrachial Nucleus (LPBN) restrains sodium intake induced by different natriorexigenic stimuli and might affect the acute response to aldosterone into the 4th V. In the present study, 1.8% NaCl and water intake was tested in rats treated with acute injections of aldosterone into the 4th V combined with the blockade of the inhibitory mechanisms with injections of moxonidine (α2 adrenergic/imidazoline agonist) or methysergide (a serotonergic antagonist) into the LPBN. Male Holtzman rats with stainless steel cannulas implanted in the 4th V and biLaterally in the LPBN were used. Aldosterone (250 or 500ng) into the 4th V combined with vehicle into the LPBN induced no 1.8% NaClintake compared to control (1.5±1.1 and 1.1±0.4, respectively, vs. vehicle into 4th V: 1.0±0.5ml/2h). However, aldosterone (250 or 500ng) into the 4th V combined with moxonidine (0.5nmol) into the LPBN induced strong ingestion of 1.8% NaCl (12.7±4.6 and 17.6±3.7ml/2h, respectively). Aldosterone (250ng) into the 4th V combined with methysergide (4μg) into the LPBN also induced 1.8% NaCl intake (17.6±5.4ml/2h). These data suggest that the inhibitory mechanisms of the LPBN counteract the facilitation of sodium intake produced by aldosterone injected into the 4th, restraining sodium intake in this condition.
-
Lateral Parabrachial Nucleus and opioid mechanisms of the central Nucleus of the amygdala in the control of sodium intake
Behavioural Brain Research, 2017Co-Authors: G M F Andradefranze, Laurival A De Luca, Debora S. A. Colombari, C.a.f. Andrade, Patricia M De Paula, Silvia Gasparini, Eduardo Colombari, José Vanderlei MenaniAbstract:Facilitatory and inhibitory mechanisms in the central Nucleus of the amygdala (CeA) and the Lateral Parabrachial Nucleus (LPBN), respectively, are important for the control of sodium and water intake. Here we investigated the importance of the opioid mechanisms in the CeA for water and 0.3 M NaCl intake in euhydrated or hyperosmotic rats treated with injections of muscimol (GABAA agonist) or moxonidine (α2 adrenergic/imidazoline agonist) into the LPBN, respectively. Male Holtzman rats (n = 4–8/group) with stainless steel cannulas implanted biLaterally in the CeA and in the LPBN were used. The ingestion of 0.3 M NaCl and water by euhydrated rats treated with muscimol (0.5 nmol/0.2 μl) into the LPBN (29.4 ± 2.7 and 15.0 ± 2.4 ml/4 h, respectively) was abolished by the previous injections of naloxone (opioid antagonist, 40 μg/0.2 μl) into the CeA (0.7 ± 0.3 and 0.3 ± 0.1 ml/4 h, respectively). The ingestion of 0.3 M NaCl by rats treated with intragastric 2 M NaCl (2 ml/rat) combined with moxonidine (0.5 nmol/0.2 μl) into the LPBN (17.0 ± 3.8 ml/2 h) was also strongly reduced by the previous injections of naloxone into the CeA (3.2 ± 2.5 ml/2 h). Sucrose intake was not affected by naloxone injections into the CeA, which minimized the possibility of non-specific inhibition of ingestive behaviors with this treatment. The present results suggest that opioid mechanisms in the CeA are essential for hypertonic NaCl intake when the LPBN inhibitory mechanisms are deactivated or attenuated with injections of muscimol or moxonidine in this area.
Laurival A De Luca - One of the best experts on this subject based on the ideXlab platform.
-
Mineral preference in rats treated with muscimol into the Lateral Parabrachial Nucleus
Neuroscience letters, 2020Co-Authors: João Carlos Callera, Laurival A De Luca, José Vanderlei MenaniAbstract:Abstract Injection of muscimol, a GABAA receptor agonist, into the Lateral Parabrachial Nucleus (LPBN) induces 0.3 M NaCl intake in rats. In the present work, we investigated whether such an effect applies to hypertonic (0.3 M) mineral solutions in general or is selective to sodium solutions in a 240 min intake test. Muscimol injection (0.5 nmol/0.2 μL) compared to vehicle injection into the LPBN of adult hydrated rats produced a preferential ingestion of 0.3 M NaCl (25.3 ± 10.2 mL) followed by a 0.3 M NaHCO3 intake (11.7 ± 5.6 mL), with no significant effect on water, KCl and CaCl2 intake. Only the effect of muscimol on NaCl intake (19.0 ± 10.4 mL) persisted in cell-dehydrated rats, with hardly any effect on water or other mineral solutions. The results suggest that the LPBN controls the ingestion of hypertonic NaCl and NaHCO3. They also suggest a selective mechanisms involving the LPBN to check hypertonic sodium intake.
-
Opioid and α2 adrenergic mechanisms are activated by GABA agonists in the Lateral Parabrachial Nucleus to induce sodium intake.
Brain Research Bulletin, 2018Co-Authors: Lisandra Brandino De Oliveira, Laurival A De Luca, Carina Aparecida Fabrício De ,andrade, Debora S. A. Colombari, José Vanderlei MenaniAbstract:Abstract The activation of GABA, opioid or α2 adrenergic mechanisms in the Lateral Parabrachial Nucleus (LPBN) facilitates hypertonic NaCl intake in rats. In the present study, we combined opioid or α2 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 α2-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 (GABAA and GABAB 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 (α2 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 α2 adrenergic mechanisms in the LPBN.
-
the Lateral Parabrachial Nucleus and central angiotensinergic mechanisms in the control of sodium intake induced by different stimuli
Behavioural Brain Research, 2017Co-Authors: Camila F Roncari, Laurival A De Luca, Debora S. A. Colombari, Patricia M De Paula, Eduardo Colombari, R B David, José Vanderlei MenaniAbstract:Abstract Angiotensin II (ANG II) is a typical facilitatory stimulus for sodium appetite. Surprisingly, hyperosmolarity and central cholinergic stimulation, two classical antinatriorexigenic stimuli, also facilitate NaCl intake when they are combined with injections of the α 2 -adrenoceptor/imidazoline agonist moxonidine into the Lateral Parabrachial Nucleus (LPBN). In the present study, we tested the relative importance of central angiotensinergic and cholinergic mechanisms for the control of water and NaCl intake by combining different dipsogenic or natriorexigenic stimuli with moxonidine injection into the LPBN. Adult male Holtzman rats (n = 9–10/group) with stainless steel cannulas implanted in the Lateral ventricle and LPBN were used. BiLateral injections of moxonidine (0.5 nmol) into the LPBN increased water and 0.3 M NaCl intake in rats that received furosemide + captopril injected subcutaneously, ANG II (50 ng) or carbachol (cholinergic agonist, 4 nmol) injected intracerebroventricularly (icv) or 2 M NaCl infused intragastrically (2 ml/rat). Losartan (AT 1 antagonist, 100 μg) or atropine (muscarinic antagonist, 20 nmol) injected icv abolished the effects on water and 0.3 M NaCl of moxonidine combined to either 2 M NaCl intragastrically or carbachol icv. However, atropine icv did not change 0.3 M NaCl intake produced by direct central action of ANG II like that induced by ANG II icv or furosemide + captopril combined with moxonidine into the LPBN. The results suggest that different stimuli, including hyperosmolarity and central cholinergic stimulation, share central angiotensinergic activation as a common mechanism to facilitate sodium intake, particularly when they are combined with deactivation of the LPBN inhibitory mechanisms.
-
Lateral Parabrachial Nucleus and opioid mechanisms of the central Nucleus of the amygdala in the control of sodium intake
Behavioural Brain Research, 2017Co-Authors: G M F Andradefranze, Laurival A De Luca, Debora S. A. Colombari, C.a.f. Andrade, Patricia M De Paula, Silvia Gasparini, Eduardo Colombari, José Vanderlei MenaniAbstract:Facilitatory and inhibitory mechanisms in the central Nucleus of the amygdala (CeA) and the Lateral Parabrachial Nucleus (LPBN), respectively, are important for the control of sodium and water intake. Here we investigated the importance of the opioid mechanisms in the CeA for water and 0.3 M NaCl intake in euhydrated or hyperosmotic rats treated with injections of muscimol (GABAA agonist) or moxonidine (α2 adrenergic/imidazoline agonist) into the LPBN, respectively. Male Holtzman rats (n = 4–8/group) with stainless steel cannulas implanted biLaterally in the CeA and in the LPBN were used. The ingestion of 0.3 M NaCl and water by euhydrated rats treated with muscimol (0.5 nmol/0.2 μl) into the LPBN (29.4 ± 2.7 and 15.0 ± 2.4 ml/4 h, respectively) was abolished by the previous injections of naloxone (opioid antagonist, 40 μg/0.2 μl) into the CeA (0.7 ± 0.3 and 0.3 ± 0.1 ml/4 h, respectively). The ingestion of 0.3 M NaCl by rats treated with intragastric 2 M NaCl (2 ml/rat) combined with moxonidine (0.5 nmol/0.2 μl) into the LPBN (17.0 ± 3.8 ml/2 h) was also strongly reduced by the previous injections of naloxone into the CeA (3.2 ± 2.5 ml/2 h). Sucrose intake was not affected by naloxone injections into the CeA, which minimized the possibility of non-specific inhibition of ingestive behaviors with this treatment. The present results suggest that opioid mechanisms in the CeA are essential for hypertonic NaCl intake when the LPBN inhibitory mechanisms are deactivated or attenuated with injections of muscimol or moxonidine in this area.
-
importance of the central Nucleus of the amygdala on sodium intake caused by deactivation of Lateral Parabrachial Nucleus
Brain Research, 2015Co-Authors: G M F Andradefranze, Laurival A De Luca, Debora S. A. Colombari, C.a.f. Andrade, Patricia M De Paula, Silvia Gasparini, Eduardo Colombari, José Vanderlei MenaniAbstract: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.
Alan Kim Johnson - One of the best experts on this subject based on the ideXlab platform.
-
Role of the Lateral Parabrachial Nucleus in the control of sodium appetite
American journal of physiology. Regulatory integrative and comparative physiology, 2014Co-Authors: José Vanderlei Menani, Laurival A De Luca, Alan Kim JohnsonAbstract:In states of sodium deficiency many animals seek and consume salty solutions to restore body fluid homeostasis. These behaviors reflect the presence of sodium appetite that is a manifestation of a pattern of central nervous system (CNS) activity with facilitatory and inhibitory components that are affected by several neurohumoral factors. The primary focus of this review is on one structure in this central system, the Lateral Parabrachial Nucleus (LPBN). However, before turning to a more detailed discussion of the LPBN, a brief overview of body fluid balance-related body-to-brain signaling and the identification of the primary CNS structures and humoral factors involved in the control of sodium appetite is necessary. Angiotensin II, mineralocorticoids, and extracellular osmotic changes act on forebrain areas to facilitate sodium appetite and thirst. In the hindbrain, the LPBN functions as a key integrative node with an ascending output that exerts inhibitory influences on forebrain regions. A nonspecific or general deactivation of LPBN-associated inhibition by GABA or opioid agonists produces NaCl intake in euhydrated rats without any other treatment. Selective LPBN manipulation of other neurotransmitter systems [e.g., serotonin, cholecystokinin (CCK), corticotrophin-releasing factor (CRF), glutamate, ATP, or norepinephrine] greatly enhances NaCl intake when accompanied by additional treatments that induce either thirst or sodium appetite. The LPBN interacts with key forebrain areas that include the subfornical organ and central amygdala to determine sodium intake. To summarize, a model of LPBN inhibitory actions on forebrain facilitatory components for the control of sodium appetite is presented in this review.
-
non nmda receptors in the Lateral Parabrachial Nucleus modulate sodium appetite
Brain Research, 2009Co-Authors: Juliana Irani Fratucci De Gobbi, José Vanderlei Menani, Robert L Thunhorst, Terry G Beltz, Ralph F Johnson, Alan Kim JohnsonAbstract:Glutamatergic mechanisms have been implicated in the control of fluid ingestion. In the present study, we investigated whether non-N-methyl-d-aspartate (NMDA) glutamatergic receptors in the Lateral Parabrachial Nucleus (LPBN) are involved in the control of water and sodium intake. Male Sprague-Dawley rats had cannulas implanted biLaterally into the LPBN. They were acutely depleted of water and sodium by injections of the diuretic furosemide (Furo; 10 mg/kg, bw) and given a low dose of the angiotensin-converting enzyme inhibitor, captopril (Cap; 5 mg/kg, bw). BiLateral LPBN injections of the non-NMDA receptor antagonist DNQX (2 and 5 nmol/0.2 microl) increased the ingestion of 0.3 M NaCl and water of Furo/Cap treated rats. The increased ingestion produced by DNQX was abolished by pretreating the LPBN with alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), a non-NMDA receptor agonist. AMPA injected alone into the LPBN reduced water and 0.3 M NaCl intake. Injections of DNQX (5 nmol/0.2 microl) into the LPBN also produced ingestion of 0.3 M NaCl after sc injections of the beta-adrenoceptor agonist, isoproterenol, a hypotensive drug that typically produces only water intake. Food intake, arterial blood pressure and heart rate were not altered by DNQX LPBN injections. We conclude that agonists acting on non-NMDA receptors in the LPBN exert an inhibitory influence on sodium intake during acute fluid depletion with hypotension and after isoproterenol treatment. A possible interaction of serotonin with glutamate within the LPBN is discussed.
-
5 ht2 and 5 ht3 receptors in the Lateral Parabrachial Nucleus mediate opposite effects on sodium intake
Neuroscience, 2007Co-Authors: Juliana Irani Fratucci De Gobbi, Alan Kim Johnson, L. A. De Luca, S. P. Barbosa, Robert L Thunhorst, Terry G Beltz, G Martinez, Vanderlei J MenaniAbstract:The present study investigated the role of several 5-HT receptor subtypes in the Lateral Parabrachial Nucleus (LPBN) in the control of sodium appetite (i.e. NaCl consumption). Male Holtzman rats had cannulas implanted biLaterally into the LPBN for the injection of 5-HT receptor agonists and antagonists in conjunction with either acute fluid depletion or 24-h sodium depletion. Following these treatments, access to 0.3 M NaCl was provided and the intakes of saline and water were measured for the next 2 h. BiLateral injections of the 5-HT2A receptor antagonist, ketanserin or the 5-HT2C receptor antagonist, mianserin into the LPBN increased 0.3 M NaCl intake without affecting water intake induced by acute fluid-depletion. BiLateral injections of the 5-HT2B receptor agonist, BW723C86 hydrochloride, had no effect on 0.3 M NaCl or water intake under these conditions. Treatment of the LPBN with the 5-HT2B/2C receptor agonist, 2-(2-methyl-4-clorophenoxy) propanoic acid (mCPP) caused dose-related reductions in 0.3 M NaCl intake after 24 h sodium depletion. The effects of mCPP were prevented by pretreating the LPBN with the 5-HT2B/2C receptor antagonist, SDZSER082. Activation of 5-HT3 receptors by the receptor agonist, 1-phenylbiguanide (PBG) caused dose-related increases in 0.3 M NaCl intake. Pretreatment of the LPBN with the 5-HT3 receptor antagonist, 1-methyl-N-[8-methyl-8-azabicyclo (3.2.1)-oct-3-yl]-1H-indazole-3-carboxamide (LY-278,584) abolished the effects of PBG, but LY-278,584 had no effects on sodium or water intake when injected by itself. PBG injected into the LPBN did not alter intake of palatable 0.06 M sucrose in fluid replete rats. The results suggest that activation of the 5-HT2A and 5-HT2C receptor subtypes inhibits sodium ingestion. In contrast, activation of the 5-HT3 receptor subtype increases sodium ingestion. Therefore, multiple serotonergic receptor subtypes in the LPBN are implicated in the control of sodium intake, sometimes by mediating opposite effects of 5-HT. The results provide new information concerning the control of sodium intake by LPBN mechanisms.
-
Corticotropin-releasing hormone in the Lateral Parabrachial Nucleus inhibits sodium appetite in rats
American journal of physiology. Regulatory integrative and comparative physiology, 2005Co-Authors: Emilio De Castro E Silva, Josmara Bartolomei Fregoneze, Alan Kim JohnsonAbstract:The present study investigated the role of corticotropin-releasing hormone (CRH) in the Lateral Parabrachial Nucleus (LPBN) in the behavioral control of body fluid homeostasis by determining the ef...
-
interaction of serotonin and cholecystokinin in the Lateral Parabrachial Nucleus to control sodium intake
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2001Co-Authors: Juliana Irani Fratucci De Gobbi, Laurival A De Luca, Alan Kim Johnson, José Vanderlei MenaniAbstract:Serotonin [5-hydroxytryptamine (5-HT)] and CCK injected into the Lateral Parabrachial Nucleus (LPBN) inhibit NaCl and water intake. In this study, we investigated interactions between 5-HT and CCK ...
Debora S. A. Colombari - One of the best experts on this subject based on the ideXlab platform.
-
Opioid and α2 adrenergic mechanisms are activated by GABA agonists in the Lateral Parabrachial Nucleus to induce sodium intake.
Brain Research Bulletin, 2018Co-Authors: Lisandra Brandino De Oliveira, Laurival A De Luca, Carina Aparecida Fabrício De ,andrade, Debora S. A. Colombari, José Vanderlei MenaniAbstract:Abstract The activation of GABA, opioid or α2 adrenergic mechanisms in the Lateral Parabrachial Nucleus (LPBN) facilitates hypertonic NaCl intake in rats. In the present study, we combined opioid or α2 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 α2-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 (GABAA and GABAB 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 (α2 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 α2 adrenergic mechanisms in the LPBN.
-
the Lateral Parabrachial Nucleus and central angiotensinergic mechanisms in the control of sodium intake induced by different stimuli
Behavioural Brain Research, 2017Co-Authors: Camila F Roncari, Laurival A De Luca, Debora S. A. Colombari, Patricia M De Paula, Eduardo Colombari, R B David, José Vanderlei MenaniAbstract:Abstract Angiotensin II (ANG II) is a typical facilitatory stimulus for sodium appetite. Surprisingly, hyperosmolarity and central cholinergic stimulation, two classical antinatriorexigenic stimuli, also facilitate NaCl intake when they are combined with injections of the α 2 -adrenoceptor/imidazoline agonist moxonidine into the Lateral Parabrachial Nucleus (LPBN). In the present study, we tested the relative importance of central angiotensinergic and cholinergic mechanisms for the control of water and NaCl intake by combining different dipsogenic or natriorexigenic stimuli with moxonidine injection into the LPBN. Adult male Holtzman rats (n = 9–10/group) with stainless steel cannulas implanted in the Lateral ventricle and LPBN were used. BiLateral injections of moxonidine (0.5 nmol) into the LPBN increased water and 0.3 M NaCl intake in rats that received furosemide + captopril injected subcutaneously, ANG II (50 ng) or carbachol (cholinergic agonist, 4 nmol) injected intracerebroventricularly (icv) or 2 M NaCl infused intragastrically (2 ml/rat). Losartan (AT 1 antagonist, 100 μg) or atropine (muscarinic antagonist, 20 nmol) injected icv abolished the effects on water and 0.3 M NaCl of moxonidine combined to either 2 M NaCl intragastrically or carbachol icv. However, atropine icv did not change 0.3 M NaCl intake produced by direct central action of ANG II like that induced by ANG II icv or furosemide + captopril combined with moxonidine into the LPBN. The results suggest that different stimuli, including hyperosmolarity and central cholinergic stimulation, share central angiotensinergic activation as a common mechanism to facilitate sodium intake, particularly when they are combined with deactivation of the LPBN inhibitory mechanisms.
-
Lateral Parabrachial Nucleus and opioid mechanisms of the central Nucleus of the amygdala in the control of sodium intake
Behavioural Brain Research, 2017Co-Authors: G M F Andradefranze, Laurival A De Luca, Debora S. A. Colombari, C.a.f. Andrade, Patricia M De Paula, Silvia Gasparini, Eduardo Colombari, José Vanderlei MenaniAbstract:Facilitatory and inhibitory mechanisms in the central Nucleus of the amygdala (CeA) and the Lateral Parabrachial Nucleus (LPBN), respectively, are important for the control of sodium and water intake. Here we investigated the importance of the opioid mechanisms in the CeA for water and 0.3 M NaCl intake in euhydrated or hyperosmotic rats treated with injections of muscimol (GABAA agonist) or moxonidine (α2 adrenergic/imidazoline agonist) into the LPBN, respectively. Male Holtzman rats (n = 4–8/group) with stainless steel cannulas implanted biLaterally in the CeA and in the LPBN were used. The ingestion of 0.3 M NaCl and water by euhydrated rats treated with muscimol (0.5 nmol/0.2 μl) into the LPBN (29.4 ± 2.7 and 15.0 ± 2.4 ml/4 h, respectively) was abolished by the previous injections of naloxone (opioid antagonist, 40 μg/0.2 μl) into the CeA (0.7 ± 0.3 and 0.3 ± 0.1 ml/4 h, respectively). The ingestion of 0.3 M NaCl by rats treated with intragastric 2 M NaCl (2 ml/rat) combined with moxonidine (0.5 nmol/0.2 μl) into the LPBN (17.0 ± 3.8 ml/2 h) was also strongly reduced by the previous injections of naloxone into the CeA (3.2 ± 2.5 ml/2 h). Sucrose intake was not affected by naloxone injections into the CeA, which minimized the possibility of non-specific inhibition of ingestive behaviors with this treatment. The present results suggest that opioid mechanisms in the CeA are essential for hypertonic NaCl intake when the LPBN inhibitory mechanisms are deactivated or attenuated with injections of muscimol or moxonidine in this area.
-
importance of the central Nucleus of the amygdala on sodium intake caused by deactivation of Lateral Parabrachial Nucleus
Brain Research, 2015Co-Authors: G M F Andradefranze, Laurival A De Luca, Debora S. A. Colombari, C.a.f. Andrade, Patricia M De Paula, Silvia Gasparini, Eduardo Colombari, José Vanderlei MenaniAbstract: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.
-
sodium intake combining cholinergic activation and noradrenaline into the Lateral Parabrachial Nucleus
Neuroscience, 2015Co-Authors: Silvia Gasparini, Carina Aparecida Fabrício De ,andrade, L. A. De Luca, Debora S. A. Colombari, Patricia M De Paula, G M F Andradefranze, Joelma Maria Cardoso Gomide, Eduardo Colombari, José Vanderlei MenaniAbstract:Abstract The administration of cholinergic agonists like pilocarpine intraperitoneally (i.p.) or carbachol intracerebroventricularly (i.c.v.) induces water, but non significant hypertonic NaCl intake. These treatments also produce pressor responses, which may inhibit sodium intake. Noradrenaline (NOR) acting on α 2 -adrenoceptors in the Lateral Parabrachial Nucleus (LPBN) deactivates inhibitory mechanisms increasing fluid depletion-induced sodium intake. In the present study, we investigated: (1) water and 1.8% NaCl intake in rats treated with pilocarpine i.p. or carbachol i.c.v. combined with NOR into the LPBN; (2) if inhibitory signals from cardiovascular receptors are blocked by NOR in the LPBN. Male Holtzman rats with stainless steel guide-cannulas implanted in the Lateral ventricle and biLaterally in the LPBN were used. BiLateral injections of NOR (80 nmol/0.2 μl) into the LPBN decreased water intake (0.8 ± 0.3, vs. saline (SAL): 2.9 ± 0.3 ml/180 min) induced by pilocarpine (1 mg/kg of body weight) i.p., without changing 1.8% NaCl intake (0.8 ± 2.4, vs. SAL: 0.5 ± 0.3 ml/180 min). Prazosin (1 mg/kg of body weight) i.p. blocked pressor responses and increased water and 1.8% NaCl intake (6.3 ± 1.7 and 14.7 ± 3.5 ml/180 min, respectively) in rats treated with pilocarpine combined with NOR into the LPBN. Prazosin i.p. also increased 1.8% NaCl intake in rats treated with carbachol i.c.v combined with NOR into the LPBN. The results suggest that different signals inhibit sodium intake in rats treated with cholinergic agonists, among them those produced by increases of arterial pressure that are not efficiently deactivated by NOR acting in the LPBN.
Marta Bianciardi - One of the best experts on this subject based on the ideXlab platform.
-
probabilistic template of the Lateral Parabrachial Nucleus medial Parabrachial Nucleus vestibular nuclei complex and medullary viscero sensory motor nuclei complex in living humans from 7 tesla mri
Frontiers in Neuroscience, 2020Co-Authors: Kavita Singh, I Indovina, Kimberly Nestor, Maria G Garciagomar, Jeffrey P Staab, Jean C Augustinack, Marta BianciardiAbstract:The Lateral Parabrachial Nucleus, medial Parabrachial Nucleus, vestibular nuclei complex and medullary viscero-sensory-motor nuclei complex (the latter including among others the solitary Nucleus, vagus nerve Nucleus, and hypoglossal Nucleus) are anatomically and functionally connected brainstem gray-matter structures that convey signals across multiple modalities between the brain and the spinal cord to regulate vital bodily functions. It is remarkably difficult to precisely extrapolate the location of these nuclei from ex vivo atlases to conventional 3 Tesla in vivo images; thus, a probabilistic brainstem template in stereotaxic neuroimaging space in living humans is needed. We delineated these nuclei using single-subject high contrast 1.1 mm isotropic resolution 7 Tesla MRI images. After precise coregistration of nuclei labels to stereotaxic space, we generated a probabilistic template of their anatomical locations. Finally, we validated the nuclei labels in the template by assessing their inter-rater agreement, consistency across subjects and volumes. We also performed a preliminary comparison of their location and microstructural properties to histologic sections of a postmortem human brainstem specimen. In future, the resulting probabilistic template of these brainstem nuclei in stereotaxic space may assist researchers and clinicians in evaluating autonomic, vestibular and viscero-sensory-motor nuclei structure, function and connectivity in living humans using conventional 3 Tesla MRI scanners.
-
Probabilistic Template of the Lateral Parabrachial Nucleus, Medial Parabrachial Nucleus, Vestibular Nuclei Complex, and Medullary Viscero-Sensory-Motor Nuclei Complex in Living Humans From 7 Tesla MRI.
Frontiers in neuroscience, 2020Co-Authors: Kavita Singh, I Indovina, Kimberly Nestor, Jeffrey P Staab, Jean C Augustinack, María G. García-gomar, Marta BianciardiAbstract:The Lateral Parabrachial Nucleus, medial Parabrachial Nucleus, vestibular nuclei complex, and medullary viscero-sensory-motor (VSM) nuclei complex (the latter including among others the solitary Nucleus, vagus nerve Nucleus, and hypoglossal Nucleus) are anatomically and functionally connected brainstem gray matter structures that convey signals across multiple modalities between the brain and the spinal cord to regulate vital bodily functions. It is remarkably difficult to precisely extrapolate the location of these nuclei from ex vivo atlases to conventional 3 Tesla in vivo images; thus, a probabilistic brainstem template in stereotaxic neuroimaging space in living humans is needed. We delineated these nuclei using single-subject high contrast 1.1 mm isotropic resolution 7 Tesla MRI images. After precise coregistration of nuclei labels to stereotaxic space, we generated a probabilistic template of their anatomical locations. Finally, we validated the nuclei labels in the template by assessing their inter-rater agreement, consistency across subjects and volumes. We also performed a preliminary comparison of their location and microstructural properties to histologic sections of a postmortem human brainstem specimen. In future, the resulting probabilistic template of these brainstem nuclei in stereotaxic space may assist researchers and clinicians in evaluating autonomic, vestibular and VSM nuclei structure, function and connectivity in living humans using conventional 3 Tesla MRI scanners.
