Local inputs to aldosterone-sensitive neurons of the nucleus tractus solitarius

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

doi:10.1016/j.neuroscience.2006.05.059

Cited by 29 publications

(33 citation statements)

References 35 publications

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“…Indeed, 11␤-hydroxylase and aldosterone synthase activity (and their encoding mRNAs, Cyp11b1 and Cyp11b2) have been found within the brain (799). In addition, 11␤-HSD2 positive neurons within the NTS are innervated by the amygdala, PVN, dorsomedial NTS, and components of the vagus (222,223,629,641), which could provide a neural rather than hormonal regulation of the system. It is likely that all of these inputs may act in conjunction with circulating aldosterone to modulate NTS control of sodium appetite.…”

Section: Central Regulation Of Blood Pressure and Salt Appetitementioning

confidence: 99%

11β-Hydroxysteroid Dehydrogenases: Intracellular Gate-Keepers of Tissue Glucocorticoid Action

Chapman

Holmes

Seckl

2013

Physiological Reviews

675

601

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Glucocorticoid action on target tissues is determined by the density of “nuclear” receptors and intracellular metabolism by the two isozymes of 11β-hydroxysteroid dehydrogenase (11β-HSD) which catalyze interconversion of active cortisol and corticosterone with inert cortisone and 11-dehydrocorticosterone. 11β-HSD type 1, a predominant reductase in most intact cells, catalyzes the regeneration of active glucocorticoids, thus amplifying cellular action. 11β-HSD1 is widely expressed in liver, adipose tissue, muscle, pancreatic islets, adult brain, inflammatory cells, and gonads. 11β-HSD1 is selectively elevated in adipose tissue in obesity where it contributes to metabolic complications. Similarly, 11β-HSD1 is elevated in the ageing brain where it exacerbates glucocorticoid-associated cognitive decline. Deficiency or selective inhibition of 11β-HSD1 improves multiple metabolic syndrome parameters in rodent models and human clinical trials and similarly improves cognitive function with ageing. The efficacy of inhibitors in human therapy remains unclear. 11β-HSD2 is a high-affinity dehydrogenase that inactivates glucocorticoids. In the distal nephron, 11β-HSD2 ensures that only aldosterone is an agonist at mineralocorticoid receptors (MR). 11β-HSD2 inhibition or genetic deficiency causes apparent mineralocorticoid excess and hypertension due to inappropriate glucocorticoid activation of renal MR. The placenta and fetus also highly express 11β-HSD2 which, by inactivating glucocorticoids, prevents premature maturation of fetal tissues and consequent developmental “programming.” The role of 11β-HSD2 as a marker of programming is being explored. The 11β-HSDs thus illuminate the emerging biology of intracrine control, afford important insights into human pathogenesis, and offer new tissue-restricted therapeutic avenues.

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Section: Central Regulation Of Blood Pressure and Salt Appetitementioning

confidence: 99%

11β-Hydroxysteroid Dehydrogenases: Intracellular Gate-Keepers of Tissue Glucocorticoid Action

Chapman

Holmes

Seckl

2013

Physiological Reviews

675

601

View full text Add to dashboard Cite

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“…Therefore, it is possible that primary afferents in the mouse cNTS terminate in the subpostremal subnucleus. Immunostaining of primary afferents using antibodies directed against neurotensin, 11-b-hydroxysteroid dehydorogenase type 2 (HSD2), or VGLUT1 (Sequeira et al, 2006;Corbett et al, 2005) could provide additional evidence for this hypothesis. Further, this suggests that the dorsal area of the cNTS (i.e., the subpostremal and mediolateral subnuclei) receives afferents and integrates peripheral information.…”

Section: Hypothetical Functional Roles Of Subnuclei In the Cntsmentioning

confidence: 99%

Quantitative and immunohistochemical analysis of neuronal types in the mouse caudal nucleus tractus solitarius: Focus on GABAergic neurons

Okada

Tashiro

Kato

et al. 2008

Journal of Chemical Neuroanatomy

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“…Experiments are needed to test these alternatives. Previous work reported that the AP neurons make "close contacts" with the aldosterone-sensitive NTS neurons that express HSD2 (37), and this observation needs confirmation with the electron microscope to establish whether these contacts represent synaptic terminals. Nevertheless, on the basis of the current anatomical evidence, it is reasonable to hypothesize that specific subsets of AP neurons may provide an "on-off" switch that regulates salt consumption.…”

Section: Discussionmentioning

confidence: 96%

“…AP has different connectional properties than the SFO or the OVLT. It innervates the nucleus tractus solitarius (NTS), ventrolateral medulla, and parabrachial region (4,37,41), and also projects to the pancreatic parasympathetic outflow system (19,23), but there has been no evidence to indicate that it connects with any of the sympathetic outflow systems. From the functional perspective, the AP affects a range of seemingly unrelated visceral functions, such as the vomiting reflex (2), cardiovascular reflexes (24), and food intake (10,11,18), but thus far, no rationale has been presented to explain why such diverse functions are modulated by this CVO.…”

mentioning

confidence: 99%

5-HT neurons of the area postrema become c-Fos-activated after increases in plasma sodium levels and transmit interoceptive information to the nucleus accumbens

Miller

Loewy

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Miller RL, Loewy AD. 5-HT neurons of the area postrema become c-Fos-activated after increases in plasma sodium levels and transmit interoceptive information to the nucleus accumbens. Am J Physiol Regul Integr Comp Physiol 306: R663-R673, 2014. First published March 5, 2014 doi:10.1152/ajpregu.00563.2013 neurons of the area postrema (AP) represent one neuronal phenotype implicated in the regulation of salt appetite. Tryptophan hydroxylase (Tryp-OH, synthetic enzyme-producing 5-HT) immunoreactive neurons in the AP of rats become c-Fos-activated following conditions in which plasma sodium levels are elevated; these include intraperitoneal injections of hypertonic saline and sodium repletion. Non-Tryp-OH neurons also became c-Fos-activated. Sodium depletion, which induced an increase in plasma osmolality but caused no significant change in the plasma sodium concentration, had no effect on the c-Fos activity in the AP. Epithelial sodium channels are expressed in the Tryp-OH-immunoreactive AP neurons, possibly functioning in the detection of changes in plasma sodium levels. Since little is known about the neural circuitry of these neurons, we tested whether the AP contributes to a central pathway that innervates the reward center of the brain. Stereotaxic injections of pseudorabies virus were made in the nucleus accumbens (NAc), and after 4 days, this viral tracer produced retrograde transneuronal labeling in the Tryp-OH and non-Tryp-OH AP neurons. Both sets of neurons innervate the NAc via a multisynaptic pathway. Besides sensory information regarding plasma sodium levels, the AP¡NAc pathway may also transmit other types of chemosensory information, such as those related to metabolic functions, food intake, and immune system to the subcortical structures of the reward system. Because these subcortical regions ultimately project to the medial prefrontal cortex, different types of chemical signals from visceral systems may influence affective functions. area postrema; circumventricular organs; epithelial sodium channels; nucleus accumbens; ventral tegmental area THE AREA POSTREMA (AP) IS a sensory circumventricular organ (CVO) located in the dorsal midline of the medulla oblongata, which protrudes into the 4th ventricle. Its terminal arterial supply is made up of fenestrated capillaries with pores measuring ϳ60 -80 nm, which allow the passage of solutes and small peptides from the plasma into the AP, so the local neurons and glial cells are bathed in a similar chemical environment as the plasma. CVO neurons detect small changes in the plasma concentration of many of these chemicals and convert this information into neural activity that is sent via feed-forward excitatory pathways to homeostatic regulatory sites in the hypothalamus. For example, the forebrain CVO neurons, originating in the subfornical organ (SFO) and organum vasculosum of the lamina terminalis (OVLT), project to the vasopressin and oxytocin neurons of the supraoptic and paraventricular hypothalamic nuclei and elicit the release of these hormones that...

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Local inputs to aldosterone-sensitive neurons of the nucleus tractus solitarius

Cited by 29 publications

References 35 publications

11β-Hydroxysteroid Dehydrogenases: Intracellular Gate-Keepers of Tissue Glucocorticoid Action

11β-Hydroxysteroid Dehydrogenases: Intracellular Gate-Keepers of Tissue Glucocorticoid Action

Quantitative and immunohistochemical analysis of neuronal types in the mouse caudal nucleus tractus solitarius: Focus on GABAergic neurons

5-HT neurons of the area postrema become c-Fos-activated after increases in plasma sodium levels and transmit interoceptive information to the nucleus accumbens

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