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André Souza Mecawi - One of the best experts on this subject based on the ideXlab platform.
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brain osmo Sodium sensitive channels and the onset of Sodium Appetite
Hormones and Behavior, 2020Co-Authors: C Y Porcari, Jose Antunesrodrigues, Ximena E. Caeiro, André Souza Mecawi, Lucas Kniess Debarba, J L Amigone, L C Reis, Thiago M Cunha, L L K Elias, Laura VivasAbstract:Abstract The aim of the present study was to determine whether the TRPV1 channel is involved in the onset of Sodium Appetite. For this purpose, we used TRPV1-knockout mice to investigate Sodium depletion-induced drinking at different times (2/24 h) after furosemide administration combined with a low Sodium diet (FURO-LSD). In Sodium depleted wild type and TRPV1 KO (SD-WT/SD-TPRV1-KO) mice, we also evaluated the participation of other Sodium sensors, such as TPRV4, NaX and angiotensin AT1-receptors (by RT-PCR), as well as investigating the pattern of neural activation shown by Fos immunoreactivity, in different nuclei involved in hydromineral regulation. TPRV1 SD-KO mice revealed an increased Sodium preference, ingesting a higher hypertonic cocktail in comparison with SD-WT mice. Our results also showed in SD-WT animals that SFO-Trpv4 expression increased 2 h after FURO-LSD, compared to other groups, thus supporting a role of SFO-Trpv4 channels during the hyponatremic state. However, the SD-TPRV1-KO animals did not show this early increase, and maybe as a consequence drank more hypertonic cocktail. Regarding the SFO-NaX channel expression, in both genotypes our findings revealed a reduction 24 h after FURO-LSD. In addition, there was an increase in the OVLT-NaX expression of SD-WT 24 h after FURO-LSD, suggesting the participation of OVLT-NaX channels in the appearance of Sodium Appetite, possibly as an anticipatory response in order to limit Sodium intake and to induce thirst. Our work demonstrates changes in the expression of different osmo‑Sodium-sensitive channels at specific nuclei, related to the body Sodium status in order to stimulate an adequate drinking.
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Sodium Appetite elicited by low-Sodium diet is dependent on p44/42 mitogen-activated protein kinase (extracellular signal-regulated kinase 1/2) activation in the brain
Journal of Neuroendocrinology, 2017Co-Authors: Lívia Da Rocha Natalino Monteiro, Paula Beatriz Marangon, L C Reis, Lucila Leico Kagohara Elias, José Antunes-rodrigues, André Souza MecawiAbstract:: Sodium Appetite is regulated by several signalling molecules, among which angiotensin II (Ang II) serves as a key driver of robust salt intake by binding to Ang II type 1 receptors (AT1R) in several regions in the brain. The activation of these receptors recruits the mitogen-activated protein kinase (MAPK) pathway, which has previously been linked to Ang II-induced increases in Sodium Appetite. Thus, we addressed the involvement of MAPK signalling in the induction of Sodium Appetite after 4 days of low-Sodium diet consumption. An increase in extracellular signal-regulated kinase (ERK) phosphorylation in the laminae terminalis and mediobasal hypothalamus was observed after low-Sodium diet consumption. This response was reduced by i.c.v. microinjection of an AT1R antagonist into the laminae terminalis but not the hypothalamus. This result indicates that low-Sodium diet consumption activates the MAPK pathway via Ang II/AT1R signalling on the laminae terminalis. On the other hand, activation of the MAPK pathway in the mediobasal hypothalamus after low-Sodium diet consumption appears to involve another extracellular mediator. We also evaluated whether a low-Sodium diet could increase the sensitivity for Ang II in the brain and activate the MAPK pathway. However, i.c.v. injection of Ang II increased ERK phosphorylation on the laminae terminalis and mediobasal hypothalamus; this increase achieved a response magnitude similar to those observed in both the normal and low-Sodium diet groups. These data indicate that low-Sodium diet consumption for 4 days is insufficient to change the ERK phosphorylation response to Ang II in the brain. To investigate whether the MAPK pathway is involved in Sodium Appetite after low-Sodium diet consumption, we performed i.c.v. microinjections of a MAPK pathway inhibitor (PD98059). PD98059 inhibited both saline and water intake after low-Sodium diet consumption. Thus, the MAPK pathway is involved in promoting the Sodium Appetite after low-Sodium diet consumption.
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Sodium Appetite elicited by low Sodium diet is dependent on p44 42 mitogen activated protein kinase extracellular signal regulated kinase 1 2 activation in the brain
Journal of Neuroendocrinology, 2017Co-Authors: Livia Monteiro, Paula Beatriz Marangon, Jose Antunesrodrigues, L C Reis, Lucila Leico Kagohara Elias, André Souza MecawiAbstract:: Sodium Appetite is regulated by several signalling molecules, among which angiotensin II (Ang II) serves as a key driver of robust salt intake by binding to Ang II type 1 receptors (AT1R) in several regions in the brain. The activation of these receptors recruits the mitogen-activated protein kinase (MAPK) pathway, which has previously been linked to Ang II-induced increases in Sodium Appetite. Thus, we addressed the involvement of MAPK signalling in the induction of Sodium Appetite after 4 days of low-Sodium diet consumption. An increase in extracellular signal-regulated kinase (ERK) phosphorylation in the laminae terminalis and mediobasal hypothalamus was observed after low-Sodium diet consumption. This response was reduced by i.c.v. microinjection of an AT1R antagonist into the laminae terminalis but not the hypothalamus. This result indicates that low-Sodium diet consumption activates the MAPK pathway via Ang II/AT1R signalling on the laminae terminalis. On the other hand, activation of the MAPK pathway in the mediobasal hypothalamus after low-Sodium diet consumption appears to involve another extracellular mediator. We also evaluated whether a low-Sodium diet could increase the sensitivity for Ang II in the brain and activate the MAPK pathway. However, i.c.v. injection of Ang II increased ERK phosphorylation on the laminae terminalis and mediobasal hypothalamus; this increase achieved a response magnitude similar to those observed in both the normal and low-Sodium diet groups. These data indicate that low-Sodium diet consumption for 4 days is insufficient to change the ERK phosphorylation response to Ang II in the brain. To investigate whether the MAPK pathway is involved in Sodium Appetite after low-Sodium diet consumption, we performed i.c.v. microinjections of a MAPK pathway inhibitor (PD98059). PD98059 inhibited both saline and water intake after low-Sodium diet consumption. Thus, the MAPK pathway is involved in promoting the Sodium Appetite after low-Sodium diet consumption.
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Developmental programing of thirst and Sodium Appetite.
Neuroscience and biobehavioral reviews, 2014Co-Authors: André Souza Mecawi, Laura Vivas, L C Reis, Ana Fabiola Macchione, Paula Nuñez, Carmen Perillan, Juan ArgüellesAbstract:Abstract Thirst and Sodium Appetite are the sensations responsible for the motivated behaviors of water and salt intake, respectively, and both are essential responses for the maintenance of hydromineral homeostasis in animals. These sensations and their related behaviors develop very early in the postnatal period in animals. Many studies have demonstrated several pre- and postnatal stimuli that are responsible for the developmental programing of thirst and Sodium Appetite and, consequently, the pattern of water and salt intake in adulthood in need-free or need-induced conditions. The literature systematically reports the involvement of dietary changes, hydromineral and cardiovascular challenges, renin–angiotensin system and steroid hormone disturbances, and lifestyle in these developmental factors. Therefore, this review will address how pre- and postnatal challenges can program lifelong thirst and Sodium Appetite in animals and humans, as well as which neuroendocrine substrates are involved. In addition, the possible epigenetic molecular mechanisms responsible for the developmental programing of drinking behavior, the clinical implications of hydromineral disturbances during pre- and postnatal periods, and the developmental origins of adult hydromineral behavior will be discussed.
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Ontogenetic role of angiontensin-converting enzyme in rats: thirst and Sodium Appetite evaluation.
Physiology & behavior, 2010Co-Authors: André Souza Mecawi, José Antunes-rodrigues, Iracema G. Araujo, Fabio Fagundes Da Rocha, Terezila Machado Coimbra, L C ReisAbstract:Abstract We investigated the influence of captopril (an angiotensin converting enzyme inhibitor) treatment during pregnancy and lactation period on hydromineral balance of the male adult offspring, particularly, concerning thirst and Sodium Appetite. We did not observe significant alterations in basal hydromineral (water intake, 0.3 M NaCl intake, volume and Sodium urinary concentration) or cardiovascular parameters in adult male rats perinatally treated with captopril compared to controls. However, male offspring rats that perinatally exposed to captopril showed a significant attenuation in water intake induced by osmotic stimulation, extracellular dehydration and beta-adrenergic stimulation. Moreover, captopril treatment during perinatal period decreased the salt Appetite induced by Sodium depletion. This treatment also attenuated thirst and Sodium Appetite aroused during inhibition of peripheral angiotensin II generation raised by low concentration of captopril in the adult offspring. Interestingly, perinatal exposure to captopril did not alter water or salt intake induced by i.c.v. administration of angiotensin I or angiotensin II. These results showed that chronic inhibition of angiotensin converting enzyme during pregnancy and lactation modifies the regulation of induced thirst and Sodium Appetite in adulthood.
L C Reis - One of the best experts on this subject based on the ideXlab platform.
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Sodium Appetite elicited by low-Sodium diet is dependent on p44/42 mitogen-activated protein kinase (extracellular signal-regulated kinase 1/2) activation in the brain
Journal of Neuroendocrinology, 2017Co-Authors: Lívia Da Rocha Natalino Monteiro, Paula Beatriz Marangon, L C Reis, Lucila Leico Kagohara Elias, José Antunes-rodrigues, André Souza MecawiAbstract:: Sodium Appetite is regulated by several signalling molecules, among which angiotensin II (Ang II) serves as a key driver of robust salt intake by binding to Ang II type 1 receptors (AT1R) in several regions in the brain. The activation of these receptors recruits the mitogen-activated protein kinase (MAPK) pathway, which has previously been linked to Ang II-induced increases in Sodium Appetite. Thus, we addressed the involvement of MAPK signalling in the induction of Sodium Appetite after 4 days of low-Sodium diet consumption. An increase in extracellular signal-regulated kinase (ERK) phosphorylation in the laminae terminalis and mediobasal hypothalamus was observed after low-Sodium diet consumption. This response was reduced by i.c.v. microinjection of an AT1R antagonist into the laminae terminalis but not the hypothalamus. This result indicates that low-Sodium diet consumption activates the MAPK pathway via Ang II/AT1R signalling on the laminae terminalis. On the other hand, activation of the MAPK pathway in the mediobasal hypothalamus after low-Sodium diet consumption appears to involve another extracellular mediator. We also evaluated whether a low-Sodium diet could increase the sensitivity for Ang II in the brain and activate the MAPK pathway. However, i.c.v. injection of Ang II increased ERK phosphorylation on the laminae terminalis and mediobasal hypothalamus; this increase achieved a response magnitude similar to those observed in both the normal and low-Sodium diet groups. These data indicate that low-Sodium diet consumption for 4 days is insufficient to change the ERK phosphorylation response to Ang II in the brain. To investigate whether the MAPK pathway is involved in Sodium Appetite after low-Sodium diet consumption, we performed i.c.v. microinjections of a MAPK pathway inhibitor (PD98059). PD98059 inhibited both saline and water intake after low-Sodium diet consumption. Thus, the MAPK pathway is involved in promoting the Sodium Appetite after low-Sodium diet consumption.
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Sodium Appetite elicited by low Sodium diet is dependent on p44 42 mitogen activated protein kinase extracellular signal regulated kinase 1 2 activation in the brain
Journal of Neuroendocrinology, 2017Co-Authors: Livia Monteiro, Paula Beatriz Marangon, Jose Antunesrodrigues, L C Reis, Lucila Leico Kagohara Elias, André Souza MecawiAbstract:: Sodium Appetite is regulated by several signalling molecules, among which angiotensin II (Ang II) serves as a key driver of robust salt intake by binding to Ang II type 1 receptors (AT1R) in several regions in the brain. The activation of these receptors recruits the mitogen-activated protein kinase (MAPK) pathway, which has previously been linked to Ang II-induced increases in Sodium Appetite. Thus, we addressed the involvement of MAPK signalling in the induction of Sodium Appetite after 4 days of low-Sodium diet consumption. An increase in extracellular signal-regulated kinase (ERK) phosphorylation in the laminae terminalis and mediobasal hypothalamus was observed after low-Sodium diet consumption. This response was reduced by i.c.v. microinjection of an AT1R antagonist into the laminae terminalis but not the hypothalamus. This result indicates that low-Sodium diet consumption activates the MAPK pathway via Ang II/AT1R signalling on the laminae terminalis. On the other hand, activation of the MAPK pathway in the mediobasal hypothalamus after low-Sodium diet consumption appears to involve another extracellular mediator. We also evaluated whether a low-Sodium diet could increase the sensitivity for Ang II in the brain and activate the MAPK pathway. However, i.c.v. injection of Ang II increased ERK phosphorylation on the laminae terminalis and mediobasal hypothalamus; this increase achieved a response magnitude similar to those observed in both the normal and low-Sodium diet groups. These data indicate that low-Sodium diet consumption for 4 days is insufficient to change the ERK phosphorylation response to Ang II in the brain. To investigate whether the MAPK pathway is involved in Sodium Appetite after low-Sodium diet consumption, we performed i.c.v. microinjections of a MAPK pathway inhibitor (PD98059). PD98059 inhibited both saline and water intake after low-Sodium diet consumption. Thus, the MAPK pathway is involved in promoting the Sodium Appetite after low-Sodium diet consumption.
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Developmental programing of thirst and Sodium Appetite.
Neuroscience and biobehavioral reviews, 2014Co-Authors: André Souza Mecawi, Laura Vivas, L C Reis, Ana Fabiola Macchione, Paula Nuñez, Carmen Perillan, Juan ArgüellesAbstract:Abstract Thirst and Sodium Appetite are the sensations responsible for the motivated behaviors of water and salt intake, respectively, and both are essential responses for the maintenance of hydromineral homeostasis in animals. These sensations and their related behaviors develop very early in the postnatal period in animals. Many studies have demonstrated several pre- and postnatal stimuli that are responsible for the developmental programing of thirst and Sodium Appetite and, consequently, the pattern of water and salt intake in adulthood in need-free or need-induced conditions. The literature systematically reports the involvement of dietary changes, hydromineral and cardiovascular challenges, renin–angiotensin system and steroid hormone disturbances, and lifestyle in these developmental factors. Therefore, this review will address how pre- and postnatal challenges can program lifelong thirst and Sodium Appetite in animals and humans, as well as which neuroendocrine substrates are involved. In addition, the possible epigenetic molecular mechanisms responsible for the developmental programing of drinking behavior, the clinical implications of hydromineral disturbances during pre- and postnatal periods, and the developmental origins of adult hydromineral behavior will be discussed.
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Ontogenetic role of angiontensin-converting enzyme in rats: thirst and Sodium Appetite evaluation.
Physiology & behavior, 2010Co-Authors: André Souza Mecawi, José Antunes-rodrigues, Iracema G. Araujo, Fabio Fagundes Da Rocha, Terezila Machado Coimbra, L C ReisAbstract:Abstract We investigated the influence of captopril (an angiotensin converting enzyme inhibitor) treatment during pregnancy and lactation period on hydromineral balance of the male adult offspring, particularly, concerning thirst and Sodium Appetite. We did not observe significant alterations in basal hydromineral (water intake, 0.3 M NaCl intake, volume and Sodium urinary concentration) or cardiovascular parameters in adult male rats perinatally treated with captopril compared to controls. However, male offspring rats that perinatally exposed to captopril showed a significant attenuation in water intake induced by osmotic stimulation, extracellular dehydration and beta-adrenergic stimulation. Moreover, captopril treatment during perinatal period decreased the salt Appetite induced by Sodium depletion. This treatment also attenuated thirst and Sodium Appetite aroused during inhibition of peripheral angiotensin II generation raised by low concentration of captopril in the adult offspring. Interestingly, perinatal exposure to captopril did not alter water or salt intake induced by i.c.v. administration of angiotensin I or angiotensin II. These results showed that chronic inhibition of angiotensin converting enzyme during pregnancy and lactation modifies the regulation of induced thirst and Sodium Appetite in adulthood.
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Role of the serotoninergic system in the Sodium Appetite control
Anais da Academia Brasileira de Ciências, 2007Co-Authors: L C ReisAbstract:The present article reviews the role of the serotoninergic system in the regulation of the Sodium Appetite. Data from the peripheral and icv administration of serotoninergic (5-HTergic) agents showed the participation of 5-HT2/3 receptors in the modulation of Sodium Appetite. These observations were extended with the studies carried out after brain serotonin depletion, lesions of DRN and during blockade of 5-HT2A/2C receptors in lateral parabrachial nucleus (LPBN). Brain serotonin depletion and lesions of DRN increased the Sodium Appetite response, in basal conditions, after Sodium depletion and hypovolemia or after beta-adrenergic stimulation as well. These observations raised the hypothesis that the suppression of ascending pathways from the DRN, possibly, 5-HTergic fibers, modifies the angiotensinergic or Sodium sensing mechanisms of the subfornical organ involved in the control of the Sodium Appetite. 5-HTergic blockade in LPBN induced to similar results, particularly those regarded to the natriorexigenic response evoked by volume depletion or increase of the hypertonic saline ingestion induced by brain angiotensinergic stimulation. In conclusion, many evidences lead to acceptation of an integrated participation resulting of an interaction, between DRN and LPBN, for the Sodium Appetite control.
José Vanderlei Menani - One of the best experts on this subject based on the ideXlab platform.
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Participation of α2 -adrenoceptors in Sodium Appetite inhibition during sickness behaviour following administration of lipopolysaccharide.
The Journal of physiology, 2015Co-Authors: Laurival A. De Luca, R.b. David, R.l. Almeida, Patricia M. De Paula, Carina A.f. Andrade, José Vanderlei MenaniAbstract:Sickness behaviour, a syndrome characterized by a general reduction in animal activity, is part of the active-phase response to fight infection. Lipopolysaccharide (LPS), an effective endotoxin to model sickness behaviour, reduces thirst and Sodium excretion, and increases neurohypophysial secretion. Here we review the effects of LPS on thirst and Sodium Appetite. Altered renal function and hydromineral fluid intake in response to LPS occur in the context of behavioural reorganization, which manifests itself as part of the syndrome. Recent data show that, in addition to its classical effect on thirst, non-septic doses of LPS injected intraperitoneally produce a preferential inhibition of intracellular thirst versus extracellular thirst. Moreover, LPS also reduced hypertonic NaCl intake in Sodium-depleted rats that entered a Sodium Appetite test. Antagonism of α2 -adrenoceptors abolished the effect of LPS on Sodium Appetite. LPS and cytokine transduction potentially recruit brain noradrenaline and α2 -adrenoceptors to control Sodium Appetite and sickness behaviour.
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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.
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Hindbrain mineralocorticoid mechanisms on Sodium Appetite.
American journal of physiology. Regulatory integrative and comparative physiology, 2012Co-Authors: Silmara Formenti, José Vanderlei Menani, Mirian Bassi, Natália Bonaka Nakamura, Guus H.m. Schoorlemmer, Eduardo ColombariAbstract:Aldosterone acting on the brain stimulates Sodium Appetite and sympathetic activity by mechanisms that are still not completely clear. In the present study, we investigated the effects of chronic i...
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water deprivation induced Sodium Appetite and differential expression of encephalic c fos immunoreactivity in the spontaneously hypertensive rat
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2010Co-Authors: Daniela T B Pereiraderderian, José Vanderlei Menani, Regina Célia Vendramini, Laurival A. De LucaAbstract:The spontaneously hypertensive rat (SHR) has an intense consumption of NaCl solution. Water deprivation (WD) followed by water intake to satiety induces partial rehydration (PR)—the WD-PR protocol—and Sodium Appetite. In the present work, WD produced similar water intake and no alterations in arterial pressure among spontaneously hypertensive rat (SHR), Wistar-Kyoto, and Holtzman strains. It also increased the number of cells with positive c-Fos immunoreactivity (Fos-IR) in the lamina terminalis and in the hypothalamic supraoptic (SON) and paraventricular (parvocellular, PVNp) nucleus in these strains. The WD and WD-PR produced similar alterations in all strains in serum osmolality and protein, plasma renin activity, and Sodium balance. The SHR ingested about 10 times more 0.3 M NaCl than normotensives strains in the Sodium Appetite test that follows WD-PR. After WD-PR, the Fos-IR persisted, elevated in the lamina terminalis of all strains but notably in the subfornical organ of the SHR. The WD-PR reversed Fos-IR in the SON of all strains and in the PVNp of SHR. It induced Fos-IR in the area postrema and in the nucleus of the solitary tract (NTS), dorsal raphe, parabrachial (PBN), pre-locus coeruleus (pre-LC), suprachiasmatic, and central amygdalar nucleus of all strains. This effect was bigger in the caudal-NTS, pre-LC, and medial-PBN of SHRs. The results indicate that WD-PR increases cell activity in the forebrain and hindbrain areas that control Sodium Appetite in the rat. They also suggest that increased cell activity in facilitatory brain areas precedes the intense 0.3 M NaCl intake of the SHR in the Sodium Appetite test.
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Water deprivation-induced Sodium Appetite
Physiology & behavior, 2010Co-Authors: Laurival A. De Luca, Daniela T. B. Pereira-derderian, Regina Célia Vendramini, R.b. David, José Vanderlei MenaniAbstract:A water deprived animal that ingests only water efficiently corrects its intracellular dehydration, but remains hypovolemic, in negative Sodium balance, and with high plasma renin activity and angiotensin II. Therefore, it is not surprising that it also ingests Sodium. However, separation between thirst and Sodium Appetite is necessary to use water deprivation as a method to understand the mechanisms subserving Sodium Appetite. For this purpose, we may use the water deprivation-partial repletion protocol, or WD-PR. This protocol allows performing a Sodium Appetite test after the rat has quenched its thirst; thus, the Sodium intake during this test cannot be confounded with a response to thirst. This is confirmed by hedonic shift and selective ingestion of Sodium solutions in the Sodium Appetite test that follows a WD-PR. The separation between thirst and Sodium Appetite induced by water deprivation permits the identification of brain states associated with Sodium intake in the Appetite test. One of these states relates to the activation of angiotensin II AT1 receptors. Other states relate to cell activity in key areas, e.g. subfornical organ and central amygdala, as revealed by immediate early gene c-Fos immunoreactivity or focal lesions. Angiotensin II apparently sensitizes the brain of the water deprived rat to produce an enhanced Sodium intake, as that expressed by spontaneously hypertensive and by young normotensive rat. The enhancement in Sodium intake produced by history of water deprivation is perhaps a clue to understand the putative salt addiction in humans. The paper represents an invited review by a symposium, award winner or keynote speaker at the Society for the Study of Ingestive Behavior [SSIB] Annual Meeting in Portland, July 2009.
Alan Kim Johnson - One of the best experts on this subject based on the ideXlab platform.
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Sensitization of Sodium Appetite: evidence for sustained molecular changes in the lamina terminalis
American journal of physiology. Regulatory integrative and comparative physiology, 2014Co-Authors: Seth W. Hurley, Zhongming Zhang, Terry G. Beltz, Baojian Xue, Alan Kim JohnsonAbstract:Animals with a history of Sodium depletions exhibit increases in salt intake, a phenomenon described as the sensitization of Sodium Appetite. Using a novel experimental design, the present experime...
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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.
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dissociation of thirst and Sodium Appetite in the furo cap model of extracellular dehydration and a role for n methyl d aspartate receptors in the sensitization of Sodium Appetite
Behavioral Neuroscience, 2013Co-Authors: Seth W. Hurley, Alan Kim JohnsonAbstract:Depletion of extracellular fluids motivates many animals to seek out and ingest water and Sodium. Animals with a history of extracellular dehydration display enhanced Sodium Appetite and in some cases thirst. The progressive increase in Sodium intake induced by repeated Sodium depletions is known as sensitization of Sodium Appetite. Administration of the diuretic and natriuretic drug, furosemide, along with a low dose of captopril (furo/cap), elicits thirst and a rapid onset of Sodium Appetite. In the present studies the furo/cap model was used to explore the physiological mechanisms of sensitization of Sodium Appetite. However, when thirst and Sodium Appetite were measured concurrently in the furo/cap model, individual rats exhibited sensitization of either thirst or Sodium Appetite. In subsequent studies, thirst and Sodium Appetite were dissociated by offering either water prior to Sodium or Sodium before water. When water and Sodium intake were dissociated in time, the furo/cap model reliably produced sensitization of Sodium Appetite. It is likely that neuroplasticity mediates this sensitization. Glutamatergic N-methyl-d-aspartate receptor (NMDA-R) activation is critical for the development of most forms of neuroplasticity. Therefore, we hypothesized that integrity of NMDA-R function is necessary for the sensitization of Sodium Appetite. Pharmacological blockade of NMDA-Rs with systemic administration of MK-801 (0.15mg/kg) prevented the sensitization of fluid intake in general when water and Sodium were offered concurrently, and prevented sensitization of Sodium intake specifically when water and Sodium intake were dissociated. The involvement of NMDA-Rs provides support for the possibility that sensitization of Sodium Appetite is mediated by neuroplasticity.
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Dissociation of thirst and Sodium Appetite in the furo/cap model of extracellular dehydration and a role for N-methyl-D-aspartate receptors in the sensitization of Sodium Appetite
Behavioral neuroscience, 2013Co-Authors: Seth W. Hurley, Alan Kim JohnsonAbstract:Depletion of extracellular fluids motivates many animals to seek out and ingest water and Sodium. Animals with a history of extracellular dehydration display enhanced Sodium Appetite and in some cases thirst. The progressive increase in Sodium intake induced by repeated Sodium depletions is known as sensitization of Sodium Appetite. Administration of the diuretic and natriuretic drug, furosemide, along with a low dose of captopril (furo/cap), elicits thirst and a rapid onset of Sodium Appetite. In the present studies the furo/cap model was used to explore the physiological mechanisms of sensitization of Sodium Appetite. However, when thirst and Sodium Appetite were measured concurrently in the furo/cap model, individual rats exhibited sensitization of either thirst or Sodium Appetite. In subsequent studies, thirst and Sodium Appetite were dissociated by offering either water prior to Sodium or Sodium before water. When water and Sodium intake were dissociated in time, the furo/cap model reliably produced sensitization of Sodium Appetite. It is likely that neuroplasticity mediates this sensitization. Glutamatergic N-methyl-d-aspartate receptor (NMDA-R) activation is critical for the development of most forms of neuroplasticity. Therefore, we hypothesized that integrity of NMDA-R function is necessary for the sensitization of Sodium Appetite. Pharmacological blockade of NMDA-Rs with systemic administration of MK-801 (0.15mg/kg) prevented the sensitization of fluid intake in general when water and Sodium were offered concurrently, and prevented sensitization of Sodium intake specifically when water and Sodium intake were dissociated. The involvement of NMDA-Rs provides support for the possibility that sensitization of Sodium Appetite is mediated by neuroplasticity.
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Behavioral cross-sensitization between DOCA-induced Sodium Appetite and cocaine-induced locomotor behavior.
Pharmacology biochemistry and behavior, 2011Co-Authors: Martin J. Acerbo, Alan Kim JohnsonAbstract:Behavioral sensitization involves increases in the magnitude of a response to a stimulus after repeated exposures to the same response initiator. Administration of psychomotor stimulants and the induction of appetitive motivational states associated with natural reinforcers like sugar and salt are among experimental manipulations producing behavioral sensitization. In rats, repeated administration of the mineralocorticoid agonist deoxycorticosterone acetate (DOCA) initially induces incremental increases in daily hypertonic saline consumption (i.e., sensitization of Sodium Appetite) in spite of the retention of Sodium. The present studies investigated whether Sodium Appetite sensitization induced by DOCA shares mechanisms similar to those of psychomotor stimulant-induced sensitization, and whether there is evidence for reciprocal cross-sensitization. In Experiments 1 and 3, rats received control or cocaine treatments to induce locomotor sensitization. A week later DOCA (or vehicle) was administered to generate a Sodium Appetite. Animals pretreated with cocaine showed a greater Sodium Appetite. In Experiment 2, the order of the putative sensitizing treatments was reversed. Rats first received either a series of DOCA or vehicle treatments either with or without access to saline and were later tested for sensitization of the locomotor response to cocaine. Animals pretreated with DOCA without access to saline showed greater locomotor responses to cocaine than animals receiving vehicle treatments. Together these experiments indicate that treatments generating a sustained salt Appetite and producing cocaine-induced psychomotor responses show reciprocal behavioral cross-sensitization. The underlying mechanisms accounting for this relationship may be the fact that psychostimulants and an unresolved craving for Sodium can act as potent stressors.
Laura Vivas - One of the best experts on this subject based on the ideXlab platform.
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brain osmo Sodium sensitive channels and the onset of Sodium Appetite
Hormones and Behavior, 2020Co-Authors: C Y Porcari, Jose Antunesrodrigues, Ximena E. Caeiro, André Souza Mecawi, Lucas Kniess Debarba, J L Amigone, L C Reis, Thiago M Cunha, L L K Elias, Laura VivasAbstract:Abstract The aim of the present study was to determine whether the TRPV1 channel is involved in the onset of Sodium Appetite. For this purpose, we used TRPV1-knockout mice to investigate Sodium depletion-induced drinking at different times (2/24 h) after furosemide administration combined with a low Sodium diet (FURO-LSD). In Sodium depleted wild type and TRPV1 KO (SD-WT/SD-TPRV1-KO) mice, we also evaluated the participation of other Sodium sensors, such as TPRV4, NaX and angiotensin AT1-receptors (by RT-PCR), as well as investigating the pattern of neural activation shown by Fos immunoreactivity, in different nuclei involved in hydromineral regulation. TPRV1 SD-KO mice revealed an increased Sodium preference, ingesting a higher hypertonic cocktail in comparison with SD-WT mice. Our results also showed in SD-WT animals that SFO-Trpv4 expression increased 2 h after FURO-LSD, compared to other groups, thus supporting a role of SFO-Trpv4 channels during the hyponatremic state. However, the SD-TPRV1-KO animals did not show this early increase, and maybe as a consequence drank more hypertonic cocktail. Regarding the SFO-NaX channel expression, in both genotypes our findings revealed a reduction 24 h after FURO-LSD. In addition, there was an increase in the OVLT-NaX expression of SD-WT 24 h after FURO-LSD, suggesting the participation of OVLT-NaX channels in the appearance of Sodium Appetite, possibly as an anticipatory response in order to limit Sodium intake and to induce thirst. Our work demonstrates changes in the expression of different osmo‑Sodium-sensitive channels at specific nuclei, related to the body Sodium status in order to stimulate an adequate drinking.
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Developmental programing of thirst and Sodium Appetite.
Neuroscience and biobehavioral reviews, 2014Co-Authors: André Souza Mecawi, Laura Vivas, L C Reis, Ana Fabiola Macchione, Paula Nuñez, Carmen Perillan, Juan ArgüellesAbstract:Abstract Thirst and Sodium Appetite are the sensations responsible for the motivated behaviors of water and salt intake, respectively, and both are essential responses for the maintenance of hydromineral homeostasis in animals. These sensations and their related behaviors develop very early in the postnatal period in animals. Many studies have demonstrated several pre- and postnatal stimuli that are responsible for the developmental programing of thirst and Sodium Appetite and, consequently, the pattern of water and salt intake in adulthood in need-free or need-induced conditions. The literature systematically reports the involvement of dietary changes, hydromineral and cardiovascular challenges, renin–angiotensin system and steroid hormone disturbances, and lifestyle in these developmental factors. Therefore, this review will address how pre- and postnatal challenges can program lifelong thirst and Sodium Appetite in animals and humans, as well as which neuroendocrine substrates are involved. In addition, the possible epigenetic molecular mechanisms responsible for the developmental programing of drinking behavior, the clinical implications of hydromineral disturbances during pre- and postnatal periods, and the developmental origins of adult hydromineral behavior will be discussed.
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Serotonergic system involvement in the inhibitory action of estrogen on induced Sodium Appetite in female rats.
Physiology & behavior, 2011Co-Authors: Carolina Dalmasso, José Luis Amigone, Laura VivasAbstract:Abstract This study of the participation of the serotonergic system in the inhibitory effect of estrogen on induced Sodium Appetite in female rats explores Sodium Appetite induced by Furosemide and low Sodium diet treatment (DEP) in normally cycling rats and in ovariectomized rats with and without estradiol replacement (OVX, OVX + E 2 ) . We also analyzed the neural activity of serotonergic neurons of the dorsal raphe nucleus (DRN) as well as the activity of other brain nuclei previously found to be involved in Sodium and water balance in Sodium depleted animals without access to the intake test. For this purpose, we examined the brain Fos, Fos-serotonin and Fos-vasopressin immunoreactivity patterns in diestrus (D), estrus (E), OVX and OVX + E 2 rats subjected to DEP. Female rats in E and OVX + E 2 exhibited a significant decrease in induced Sodium intake compared with females in D and OVX. This estrogen-dependent inhibition on induced Sodium Appetite (approximately 50% reduction) can be correlated with changes in Fos activation observed in the organum vasculosum of the lamina terminalis (OVLT) and DRN, in response to Sodium depletion. Given our previous observations in males, the expected Sodium depletion-induced activity of the OVLT was found to be absent in OVX + E 2 females, while the usual inhibitory tonic activity of serotonergic neurons of the DRN, instead of decreasing after Sodium depletion, increases or remains unchanged in OVX + E 2 -DEP and E-DEP females, respectively. Regarding urinary water and Sodium excretion 3 h after furosemide treatment, E-DEP and OVX + E 2 -DEP animals excreted smaller volumes of more highly concentrated urine than depleted D and OVX rats. Twenty hours after Sodium depletion, the same groups of animals also showed a significant increase in the number of Fos-AVP immunoreactive neurons within the supraoptic nucleus, compared with D-DEP. In summary, our results demonstrate an estrogen-dependent inhibition of induced Sodium Appetite in normally cycling rats and ovariectomized animals with estradiol replacement, which may involve an interaction between excitatory neurons of the OVLT and inhibitory serotonergic cells of the DRN. The main finding is thus serotonergic system involvement as a possible mechanism in the inhibitory action of estrogen on induced Sodium Appetite.
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Activation of lateral parabrachial afferent pathways and endocrine responses during Sodium Appetite regulation.
Experimental Neurology, 2009Co-Authors: Andrea Godino, Lisandra Oliveira Margatho, Ximena E. Caeiro, José Antunes-rodrigues, Laura VivasAbstract:Abstract Modulation of salt Appetite involves interactions between the circumventricular organs (CVOs) receptive areas and inhibitory hindbrain serotonergic circuits. Recent studies provide support to the idea that the serotonin action in the lateral parabrachial nucleus (LPBN) plays an important inhibitory role in the modulation of Sodium Appetite. The aim of the present work was to identify the specific groups of neurons projecting to the LPBN that are activated in the course of Sodium Appetite regulation, and to analyze the associated endocrine response, specifically oxytocin (OT) and atrial natriuretic peptide (ANP) plasma release, since both hormones have been implicated in the regulatory response to fluid reestablishment. For this purpose we combined the detection of a retrograde transported dye, Fluorogold (FG) injected into the LPBN with the analysis of the Fos immunocytochemistry brain pattern after Sodium intake induced by Sodium depletion. We analyzed the Fos-FG immunoreactivity after Sodium ingestion induced by peritoneal dialysis (PD). We also determined OT and ANP plasma concentration by radioimmunoassay (RIE) before and after Sodium intake stimulated by PD. The present study identifies specific groups of neurons along the paraventricular nucleus, central extended amygdala, insular cortex, dorsal raphe nucleus, nucleus of the solitary tract and the CVOs that are activated during the modulation of Sodium Appetite and have direct connections with the LPBN. It also shows that OT and ANP are released during the course of Sodium satiety and fluid reestablishment. The result of this brain network activity may enable appropriate responses that re-establish the body fluid balance after induced Sodium consumption.
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Reduced Sodium Appetite and increased oxytocin gene expression in mutant mice lacking β-endorphin
Neuroscience, 2003Co-Authors: Lucía F. Franchini, Marcelo Rubinstein, Laura VivasAbstract:Abstract Central opioid and oxytocinergic systems have been involved in the regulatory control of Sodium Appetite. In addition, previous studies support the existence of a functional interaction between opioid peptides and oxytocinergic pathways, and suggest that β-endorphin neurons would modulate the activity of central oxytocinergic pathways, its pituitary secretion and Sodium Appetite. To investigate the role of this opioid peptide in the control of oxytocin (OT) synthesis and Sodium Appetite regulation we used mice with gene dosage-dependent variations in brain β-endorphin content, expressing either 100%, 50%, or 0% of normal β-endorphin content. Our results show that β-endorphin knockout (KO) and heterozygous (HT) mutant mice consume approximately a 50% less 2% NaCl solution compared with wild type mice (WT), after furosemide and low Sodium diet treatment. These data suggest that β-endorphin may facilitate induced Sodium Appetite, giving new evidence about the role of β-endorphin on Sodium Appetite behavior. Our data also indicate that OT mRNA levels evaluated by in situ hybridization significantly increased within the hypothalamic paraventricular nucleus of WT animals after induced Sodium ingestion, giving support to former evidence indicating an inhibitory role for central OT in the control of Sodium Appetite. Moreover, β-endorphin mutated mice have similar higher levels of OT mRNA expression after the different conditions analyzed: basal, control or experimental, compared with WT mice. Both control HT and KO mice showed higher OT mRNA expression levels than control WT group and these levels did not change after induced Sodium intake. Taken together, our data suggest that the reduced Sodium ingestion observed in β-endorphin deficient mice could be due to a higher expression of the OT gene. This conclusion would support the hypothesis that OT inhibits Sodium intake and provides new evidence about β-endorphin modulation of OT synthesis and Sodium Appetite.