Bidirectional Anticipation of Future Osmotic Challenges by Vasopressin Neurons

Mandelblat-Cerf, Yael; Kim, Angela; Burgess, Christian R.; Subramanian, Siva; Tannous, Bakhos A.; Lowell, Bradford B.; Andermann, Mark L.

doi:10.1016/j.neuron.2016.11.021

Cited by 74 publications

(80 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In response to small increases in plasma osmolality, vasopressin release occurs before thirst is triggered. This neuroendocrine hormone system could be an important contributor to the endogenous rhythmical free water accrual and its modulation by dietary salt we observed in our subjects (36)(37)(38). Summary.…”

Section: Hypothesis 2: Dietary Salt Modulates Endogenous Infradianrhymentioning

confidence: 68%

Increased salt consumption induces body water conservation and decreases fluid intake

Rakova¹,

Kitada²,

Lerchl³

et al. 2017

Journal of Clinical Investigation

134

122

View full text Add to dashboard Cite

BACKGROUND. The idea that increasing salt intake increases drinking and urine volume is widely accepted. We tested the hypothesis that an increase in salt intake of 6 g/d would change fluid balance in men living under ultra-long-term controlled conditions. METHODS.Over the course of 2 separate space flight simulation studies of 105 and 205 days' duration, we exposed 10 healthy men to 3 salt intake levels (12, 9, or 6 g/d). All other nutrients were maintained constant. We studied the effect of salt-driven changes in mineralocorticoid and glucocorticoid urinary excretion on day-to-day osmolyte and water balance. RESULTS.A 6-g/d increase in salt intake increased urine osmolyte excretion, but reduced free-water clearance, indicating endogenous free water accrual by urine concentration. The resulting endogenous water surplus reduced fluid intake at the 12-g/d salt intake level. Across all 3 levels of salt intake, half-weekly and weekly rhythmical mineralocorticoid release promoted free water reabsorption via the renal concentration mechanism. Mineralocorticoid-coupled increases in free water reabsorption were counterbalanced by rhythmical glucocorticoid release, with excretion of endogenous osmolyte and water surplus by relative urine dilution. A 6-g/d increase in salt intake decreased the level of rhythmical mineralocorticoid release and elevated rhythmical glucocorticoid release. The projected effect of salt-driven hormone rhythm modulation corresponded well with the measured decrease in water intake and an increase in urine volume with surplus osmolyte excretion. CONCLUSION.Humans regulate osmolyte and water balance by rhythmical mineralocorticoid and glucocorticoid release, endogenous accrual of surplus body water, and precise surplus excretion.

show abstract

Section: Hypothesis 2: Dietary Salt Modulates Endogenous Infradianrhymentioning

confidence: 68%

Increased salt consumption induces body water conservation and decreases fluid intake

Rakova¹,

Kitada²,

Lerchl³

et al. 2017

Journal of Clinical Investigation

134

122

View full text Add to dashboard Cite

show abstract

“…This anticipation of future as well as present needs is a common feature of adaptive regulation of many physiologic variables (Somjen, 1992; Woods and Ramsay, 2007), and in the cardiovascular field has been termed feedforward homeostatic control (Dampney, 2016). In this light, the recently discovered food/water cue-based and circadian control of AgRP hunger neurons, subfornical (SFO) and organum vasculosum of the lamina terminalis (OVLT) thirst neurons, and water-excretion controlling vasopressin neurons, to be discussed later in greater detail, could be viewed as serving anticipatory, feedforward “homeostatic” functions (Betley et al, 2015; Chen et al, 2015; Gizowski et al, 2016; Mandelblat-Cerf et al, 2017; Mandelblat-Cerf et al, 2015; Zimmerman et al, 2016). …”

Section: Section 1: Clarificationsmentioning

confidence: 99%

Toward a Wiring Diagram Understanding of Appetite Control

Andermann

Lowell

2017

Neuron

Self Cite

459

396

View full text Add to dashboard Cite

Prior mouse genetic research has set the stage for a deep understanding of appetite regulation. This goal is now being realized through the use of recent technological advances, such as the ability to map connectivity between neurons, manipulate neural activity in real time, and measure neural activity during behavior. Indeed, major progress has been made with regards to meal-related gut control of appetite, arcuate nucleus-based hypothalamic circuits linking energy state to the motivational drive, hunger, and finally limbic and cognitive processes that bring about hunger-mediated increases in reward value and perception of food. Unexpected findings are also being made, for example, the rapid regulation of homeostatic neurons by cues that predict future food consumption. The aim of this review is to 1) to cover the major underpinnings of appetite regulation, 2) to describe recent advances resulting from the new technologies, and 3) to synthesize these findings into an updated view of appetite regulation.

show abstract

“…Instead, this behavior appears to anticipate homeostatic changes before they occur [13]. Anticipatory signals for thirst and vasopressin release converge on the same homeostatic neurons, subfornical organ neurons, which monitor the tonicity of blood [14,15]. The activity of subfornical organ excitatory neurons (SFO Nos1 ; Fig.…”

Section: Extero-sensory Stimulation Anticipates Thirst Stimulation Anmentioning

confidence: 99%

“…Using electrophysiological recordings (i.e., of genetically identified SON pituitaryprojecting vasopressin (VP pp ) neurons in water-restricted mice), Mandelblat-Cerf et al [15] observed rapid decreases in neuron activity within seconds of presentation of cues signaling water availability, prior to water ingestion. In contrast, ingestion of dry food -a hyperosmotic challenge -elicited rapid increases in VP pp neuron activity prior to any increase of plasma osmolality.…”

Section: Coordination Of Eating Drinking and Vasopressin Releasementioning

confidence: 99%

Vasopressin and the Regulation of Thirst

Bichet¹

2018

Ann Nutr Metab

View full text Add to dashboard Cite

Recent experiments using optogenetic tools allow the identification and functional analysis of thirst neurons and vasopressin producing neurons. Two major advances provide a detailed anatomy of taste for water and arginine-vasopressin (AVP) release: (1) thirst and AVP release are regulated not only by the classical homeostatic, intero-sensory plasma osmolality negative feedback, but also by novel, extero-sensory, anticipatory signals. These anticipatory signals for thirst and vasopressin release converge on the same homeostatic neurons of circumventricular organs that monitor the composition of the blood; (2) acid-sensing taste receptor cells (which express polycystic kidney disease 2-like 1 protein) on the tongue that were previously suggested as the sour taste sensors also mediate taste responses to water. The tongue has a taste for water. The median preoptic nucleus (MnPO) of the hypothalamus could integrate multiple thirst-generating stimuli including cardiopulmonary signals, osmolality, angiotensin II, oropharyngeal and gastric signals, the latter possibly representing anticipatory signals. Dehydration is aversive and MnPO neuron activity is proportional to the intensity of this aversive state.

show abstract

Bidirectional Anticipation of Future Osmotic Challenges by Vasopressin Neurons

Cited by 74 publications

References 38 publications

Increased salt consumption induces body water conservation and decreases fluid intake

Increased salt consumption induces body water conservation and decreases fluid intake

Toward a Wiring Diagram Understanding of Appetite Control

Vasopressin and the Regulation of Thirst

Contact Info

Product

Resources

About