Increased number of aldosterone-sensitive NTS neurons in Dahl salt-sensitive rats

Geerling, Joel C.; Sequeira, Sunitha M.; Loewy, A.

doi:10.1016/j.brainres.2005.10.044

Cited by 7 publications

(9 citation statements)

References 23 publications

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“…Although circumstances involving chronic changes in mineralocorticoid levels (such as chronic sodium deprivation, adrenalectomy, or daily mineralocorticoid injections) can influence the intensity of HSD2 immunoreactivity, changing the number of HSD2 neurons visible for counting (see Refs. 20,21), no consistent group differences were found in the present experiments.…”

Section: Methodscontrasting

confidence: 48%

Sodium depletion activates the aldosterone-sensitive neurons in the NTS independently of thirst

Geerling

Loewy²

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Thirst and sodium appetite are both critical for restoring blood volume. Because these two behavioral drives can arise under similar physiological conditions, some of the brain sensory sites that stimulate thirst may also drive sodium appetite. However, the physiological and temporal dynamics of these two appetites exhibit clear differences, suggesting that they involve separate brain circuits. Unlike thirst-associated sensory neurons in the hypothalamus, the 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2) neurons in the rat nucleus tractus solitarius (NTS) are activated in close association with sodium appetite (16). Here, we tested whether the HSD2 neurons are also activated in response to either of the two physiological stimuli for thirst: hyperosmolarity and hypovolemia. Hyperosmolarity, produced by intraperitoneal injection of hypertonic saline, stimulated a large increase in water intake and a substantial increase in immunoreactivity for the neuronal activity marker c-Fos within the medial NTS, but not in the HSD2 neurons. Hypovolemia, produced by subcutaneous injection of hyperoncotic polyethylene glycol (PEG), stimulated an increase in water intake within 1-4 h without elevating c-Fos expression in the HSD2 neurons. The HSD2 neurons were, however, activated by prolonged hypovolemia, which also stimulated sodium appetite. Twelve hours after PEG was injected in rats that had been sodium deprived for 4 days, the HSD2 neurons showed a consistent increase in c-Fos immunoreactivity. In summary, the HSD2 neurons are activated specifically in association with sodium appetite and appear not to function in thirst.

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Section: Methodscontrasting

confidence: 48%

Sodium depletion activates the aldosterone-sensitive neurons in the NTS independently of thirst

Geerling

Loewy²

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This increase in HSD2-immunoreactivity, which presumably reflects an increase in protein expression driven by elevated levels of aldosterone (Geerling et al, 2005; Geerling and Loewy, 2006c; Geerling and Loewy, 2007b), allows a complete and consistent visualization of the neurons and their dendritic arbors. As in our previous experiments, rats were housed individually during sodium deprivation with daily cage changes to prevent any re-ingestion of excreted sodium.…”

Section: Methodsmentioning

confidence: 99%

Vagal innervation of the aldosterone-sensitive HSD2 neurons in the NTS

2009

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The nucleus of the solitary tract (NTS) contains a unique subpopulation of aldosterone-sensitive neurons. These neurons express the enzyme 11-β-hydroxysteroid dehydrogenase type 2 (HSD2) and are activated by sodium deprivation. They are located in the caudal NTS, a region which is densely innervated by the vagus nerve, suggesting that they could receive direct viscerosensory input from the periphery. To test this possibility, we injected the highly sensitive axonal tracer biotinylated dextran amine (BDA) into the left nodose ganglion in rats. Using confocal microscopy, we observed a sparse input from the vagus to most HSD2 neurons. Roughly 80% of the ipsilateral HSD2 neurons exhibited at least one close contact with a BDA-labeled vagal bouton, although most of these cells received only a few total contacts. Most of these contacts were axo-dendritic (~80%), while ~20% were axo-somatic. In contrast, the synaptic vesicular transporters VGLUT2 or GAD7 labeled much larger populations of boutons contacting HSD2-labeled dendrites and somata, suggesting that direct input from the vagus may only account for a minority of the information integrated by these neurons. In summary, the aldosterone-sensitive HSD2 neurons in the NTS appear to receive a small amount of direct viscerosensory input from the vagus nerve. The peripheral sites of origin and functional significance of this projection remain unknown. Combined with previously-identified central sources of input to these cells, the present finding indicates that the HSD2 neurons integrate humoral information with input from a variety of neural afferents.

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“…Ascertaining the mechanism leading to specificity of the MR for aldosterone in non‐epithelial aldosterone target tissues has been more complicated. In situ hybridization has demonstrated mRNA for 11β‐HSD2, 11β‐HSD1, MR and glucocorticoid receptor in several areas of the brain 52–55 . However, although 11β‐HSD2 and MR mRNA were closely associated in the kidney, such an association was not found in the brain 52,53 .…”

Section: Mineralocorticoid Receptor Ligand Specificity In the Brainmentioning

confidence: 99%

Role of mineralocorticoid action in the brain in salt‐sensitive hypertension

Oki

Gómez-Sánchez

2011

Clin Exp Pharma Physio

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Summary 1. The mechanisms by which excessive salt causes hypertension involve more than retention of sodium and water by the kidneys and are far from clear. Mineralocorticoids act centrally to increase salt appetite, sympathetic drive and vasopressin release, resulting in hypertension that is prevented by the central infusion of mineralocorticoid receptor (MR) antagonists. The MR has similar affinity for aldo and the glucocorticoids corticosterone or cortisol. Specificity is conferred in transport epithelia by the co-localization of the MR with 11β-hydroxysteroid dehydrogenase type 2. Co-expression also occurs in some neurons, notably those of the nucleus tractus solitarius that are activated by sodium depletion and aldo and mediate salt seeking behavior. 2. The salt-induced hypertension of the Dahl Salt Sensitive rat is mitigated by the central infusion of a mineralocorticoid antagonist even though circulating aldo is normal or reduced in SS. Contrary to reports that salt appetite in the SS rat is depressed, we found that it is increased compared to the Spraque-Dawley (SD). 3. Extra-adrenal aldo synthesis in the brain occurs in minute amounts that could only be relevant locally. mRNA for aldo synthase enzyme and aldo concentration in the brain of the Dahl SS are increased compared to SD rats. The central infusion of inhibitors of aldo synthesis lowers salt-induced hypertension in the SS, suggesting a role for excessive aldo synthesis in the brain. Brain MR, particularly those in the PVN, regulate inflammatory processes that are exacerbated by sodium and lead to cardiovascular dysfunction.

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Increased number of aldosterone-sensitive NTS neurons in Dahl salt-sensitive rats

Cited by 7 publications

References 23 publications

Sodium depletion activates the aldosterone-sensitive neurons in the NTS independently of thirst

Sodium depletion activates the aldosterone-sensitive neurons in the NTS independently of thirst

Vagal innervation of the aldosterone-sensitive HSD2 neurons in the NTS

Role of mineralocorticoid action in the brain in salt‐sensitive hypertension

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