Vasopressin and the Regulation of Thirst

Abstract

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.

The use of mentholated popsicle to reduce thirst during preoperative fasting: A randomised controlled trial

“…Once the person is thirsty, the human organism has two mechanisms to achieve satiety: pre-and postabsorptive. Preabsorptive satiety is related to baroreceptors, osmoreceptors and thermoreceptors localised in the oropharynx, as well as to gastric receptors that act as measuring instruments of the ingested volume, even before there is absorption of the liquid (Bichet, 2018;Eccles, Du-Plessis, Dommels, & Wilkinson, 2013;Zimmerman, Leib, & Knight, 2017;Zimmerman et al, 2016). These receptors can be active by the humidification of the oral mucosa, by the mechanical process of swallowing and by the gastric distention due to the ingestion of liquids, resulting in satiety (Saker, Farrell, Adib, McKinley, & Denton, 2014;Zimmerman et al, 2016).…”

Behavioral role of PACAP signaling reflects its selective distribution in glutamatergic and GABAergic neuronal subpopulations

“…Optogenetic activation of SFO-GLUT neurons stimulates intensive drinking in hydrated mice, whereas optogenetic silencing of SFO-GLUT neurons suppresses drinking in dehydrated mice (Zimmerman, Leib et al 2017). By contrast, optogenetic activation of SFO-GABA neurons suppresses drinking in dehydrated mice (Bichet 2018). SFO-GLUT projections to the median preoptic nucleus (MnPO) and OVLT drive thirst, whereas SFO-GLUT projections to the ventrolateral part of the bed nucleus of the stria terminalis (BNSTvl) promote sodium consumption (Zimmerman, Leib et al 2017).…”

Thirst and Drinking Paradigms: Evolution from Single Factor Effects to Brainwide Dynamic Networks

“…[33,[54][55][56] Cardiovascular feedback to the brain (i.e., volume, pressure, osmolality) modulates thirst. [33,[57][58][59][60][61][62][63] A control model of thirst was developed on the basis of physiological research and was simulated using a digital computer. [64,65] The renin-angiotensin system mediates thirst and stimulates a search for water.…”

“…The rodent model of thirst and drinking behavior [63,93,151] has allowed identification of neurons that relay information regarding the status of plasma volume, vascular perfusion pressure, angiotensin II, ingested water passing through the mouth and throat, gastrointestinal water, extracellular sodium concentration and osmolality. Figure 5 illustrates and summarizes the findings of five rodent model publications which focused on thirst, thirst-related motivation, drinking behavior, and downstream signals to other brain loci.…”