Brain osmo-sodium sensitive channels and the onset of sodium appetite

Porcari, C.Y.; Debarba, Lucas Kniess; Amigone, J.L.; Caeiro, Ximena E.; Reis, L. C.; Cunha, Thiago M.; Mecawi, André Souza; Elias, Lucila Leico Kagohara; Antunes‐Rodrigues, José; Vivas, Laura; Godino, Andrea

doi:10.1016/j.yhbeh.2019.104658

Cited by 7 publications

(15 citation statements)

References 33 publications

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“…The OXT neural activity of supraoptic and paraventricular cells (SON and PVN, respectively) is implicated in the hypertonicity signaling after induced sodium intake (24 h after sodium depletion) since these are intrinsically osmosensors due to the presence of transient receptor potential channel 1 (TRPV1), like OVLT and SFO circumventricular organs (CVOs) 27 , 32 . Thus, as recently reported, TRPV1 KO mice have increased sodium preference after sodium depletion 33 .…”

Section: Introductionsupporting

confidence: 72%

“…Each brain structure presents different temporal patterns of adaptation to provide a proper response. For example, in the SFO of mice, we observed an increase in TRPV4 expression during the first hours after SD 32 , 33 . Still, later, when SA appeared, the NaX channel expression decreased (involved in the hypernatremic detection) 33 , 63 .…”

Section: Discussionmentioning

confidence: 82%

“…Our recent results showed that the TRPV1 channel, implicated in central osmosensation, is essential to the sodium preference induced by SD 33 . Osmosensation in response to changes in sodium balance is detected by the CVOs of the lamina terminalis, including SFO and OVLT, and the Oxytocin or vasopressin magnocellular cells, whose osmosensitivity relies on the presence of this channel 32 .…”

Section: Resultsmentioning

confidence: 88%

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Molecular neurobiological markers in the onset of sodium appetite

Porcari

Cambiasso

Mecawi

et al. 2022

Sci Rep

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Sodium appetite is a motivational state involving homeostatic behavior, seeking the ingest of salty substances after sodium loss. There is a temporal dissociation between sodium depletion (SD) and the appearance of sodium appetite. However, the responsible mechanisms for this delay remain poorly elucidated. In the present study, we measured the temporal changes at two and 24 h after SD in the gene expression of key elements within excitatory, inhibitory, and sensory areas implicated in the signaling pathways involved in the onset of sodium appetite. In SD rats, we observed that the expression of critical components within the brain control circuit of sodium appetite, including Angiotensin-type-1 receptor (Agtr1a), Oxytocin-(OXT-NP)-neurophysin-I, and serotonergic-(5HT)-type-2c receptor (Htr2c) were modulated by SD, regardless of time. However, we observed reduced phosphorylation of mitogen-activated protein kinases (MAPK) at the paraventricular nucleus (PVN) and increased oxytocin receptor (Oxtr) mRNA expression at the anteroventral of the third ventricle area (AV3V), at two hours after SD, when sodium appetite is inapparent. At twenty-four hours after SD, when sodium appetite is released, we observed a reduction in the mRNA expression of the transient receptor potential channel 1gene (Trpv1) and Oxtr in the AV3V and the dorsal raphe nucleus, respectively. The results indicate that SD exerts a coordinated timing effect, promoting the appearance of sodium appetite through changes in MAPK activity and lower Trpv1 channel and Oxtr expression that trigger sodium consumption to reestablish the hydroelectrolytic homeostasis.

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Section: Introductionsupporting

confidence: 72%

Section: Discussionmentioning

confidence: 82%

Section: Resultsmentioning

confidence: 88%

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Molecular neurobiological markers in the onset of sodium appetite

Porcari

Cambiasso

Mecawi

et al. 2022

Sci Rep

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“…Our data also show that sodium depletion induces larger hypertonic saline intake than the animals actually need to reestablish their hydromineral balance, since both urinary volume and sodium excretion were increased along the hypertonic saline intake test. This pronounced increased sodium appetite after 24 h of sodium depletion is induced by redundant neuroendocrine adaptations to ensure the animals reestablish their body sodium, such as the sodium and osmosensors [34,35], RAAS activation [36][37][38], changes in sodium palatability [29], decreased dorsal raphe serotonin [9,26,35,39] and hypothalamic OXT [40,41] production and activity, amongst others. In fact, our data demonstrate increased levels of circulating ANG II, indicating that the sodium appetite induced by body sodium depletion maybe, at least in part, induced by circulating ANG II by acting on AT1 receptors located in the lamina terminalis, in particular in the organum vasculosum of the lamina terminalis and the subfornical organ, that are critical for maintaining body fluid homeostasis [32,42].…”

Section: Discussionmentioning

confidence: 99%

Physiological and Transcriptomic Changes in the Hypothalamic-Neurohypophysial System after 24 h of Furosemide-Induced Sodium Depletion

Dutra¹,

Paterson²,

Monteiro³

et al. 2020

Neuroendocrinology

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Background/Aims: Furosemide is a loop diuretic widely used in clinical practice for the treatment of oedema and hypertension. The aim of this study was to determine physiological and molecular changes in the hypothalamic-neurohypophysial system as a consequence of furosemide-induced sodium depletion. Methods: Male rats were sodium depleted by acute furosemide injection (10 and 30 mg/kg) followed by access to low sodium diet and distilled water for 24 h. The renal and behavioural consequences were evaluated, while blood and brains were collected to evaluate the neuroendocrine and gene expression responses. Results: Furosemide treatment acutely increases urinary sodium and water excretion. After 24 h, water and food intake were reduced, while plasma angiotensin II and corticosterone were increased. After hypertonic saline presentation, sodium-depleted rats showed higher preference for salt. Interrogation using RNA sequencing revealed the expression of 94 genes significantly altered in the hypothalamic paraventricular nucleus (PVN) of sodium-depleted rats (31 upregulated and 63 downregulated). Out of 9 genes chosen, 5 were validated by quantitative PCR in the PVN (upregulated: Ephx2, Ndnf and Vwf; downregulated: Caprin2 and Opn3). The same genes were also assessed in the supraoptic nucleus (SON, upregulated: Tnnt1, Mis18a, Nr1d1 and Dbp; downregulated: Caprin2 and Opn3). As a result of these plastic transcriptome changes, vasopressin expression was decreased in PVN and SON, whilst vasopressin and oxytocin levels were reduced in plasma. Conclusions: We thus have identified novel genes that might regulate vasopressin gene expression in the hypothalamus controlling the magnocellular neurons secretory response to body sodium depletion and consequently hypotonic stress.

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“…Both TRPV1 and TRPV4 channels can be activated by lipid-derived molecules like arachidonic acid [ 84 , 85 ] and by a variety of toxins (e.g., scorpion venom, botulinum neurotoxin and lipopolysaccharides) [ 94 , 95 ] and play important roles in mechano-, thermo-, osmo- and nociception depending on their cell type expression [ 67 , 96 , 97 , 98 , 99 , 100 ].…”

Section: Heteromeric Trpv1/4 Assemblymentioning

confidence: 99%

Heteromeric TRP Channels in Lung Inflammation

Zergane

Kuebler

Michalick

2021

Cells

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Activation of Transient Receptor Potential (TRP) channels can disrupt endothelial barrier function, as their mediated Ca2+ influx activates the CaM (calmodulin)/MLCK (myosin light chain kinase)-signaling pathway, and thereby rearranges the cytoskeleton, increases endothelial permeability and thus can facilitate activation of inflammatory cells and formation of pulmonary edema. Interestingly, TRP channel subunits can build heterotetramers, whereas heteromeric TRPC1/4, TRPC3/6 and TRPV1/4 are expressed in the lung endothelium and could be targeted as a protective strategy to reduce endothelial permeability in pulmonary inflammation. An update on TRP heteromers and their role in lung inflammation will be provided with this review.

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Brain osmo-sodium sensitive channels and the onset of sodium appetite

Cited by 7 publications

References 33 publications

Molecular neurobiological markers in the onset of sodium appetite

Molecular neurobiological markers in the onset of sodium appetite

Physiological and Transcriptomic Changes in the Hypothalamic-Neurohypophysial System after 24 h of Furosemide-Induced Sodium Depletion

Heteromeric TRP Channels in Lung Inflammation

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