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1 rrent internal motivational state (hunger or thirst).
2 ng about financial security and experiencing thirst).
3 ted with increased AVP levels and suppressed thirst.
4 e subfornical organ that trigger or suppress thirst.
5 g overdrinking compared with drinking during thirst.
6 hese responses correlated significantly with thirst.
7 e level of water in a pitcher and quench its thirst.
8 ve, similar to temperature, itch, hunger and thirst.
9 by drinking inherent in the consciousness of thirst.
10 ng to physiological state, such as hunger or thirst.
11 r liver is necessary for sodium appetite and thirst.
12 nd elicit concordant responses to hunger and thirst.
13 al osmolality changes, and how they modulate thirst.
14 and while they imagined drinking to satiate thirst.
15 physiological deficiency states: hunger and thirst.
16 uple osmolyte retention with potentiation of thirst.
17 h imagined thirst and physiologically evoked thirst.
18 r substrates that underlie distinct types of thirst.
19 n response to dehydration, humans experience thirst.
20 owing motivational shifts between hunger and thirst.
21 large volumes of dilute urine and persistent thirst.
22 and thalamus after overdrinking, relative to thirst.
23 e signals and oppositely regulate hunger and thirst.
24 creased in the papilla of mice after 36 h of thirsting.
25 +/- 22% in the papilla of mice after 36 h of thirsting.
26 253% (P < 0.01) in the papilla upon 36 h of thirsting.
27 ncreased further in the papilla upon 36 h of thirsting.
31 patient well-being, measured as preoperative thirst, amount of fluid ingested, postoperative nausea a
33 and arginine-vasopressin (AVP) release: ( a) Thirst and AVP release are regulated by the classical ho
36 ed NaCl and AngII concentrations to regulate thirst and body fluid homeostasis.SIGNIFICANCE STATEMENT
41 the early phase of sepsis features impaired thirst and enhanced vasopressin release, the basis for t
42 lling is not required for sodium appetite or thirst and highlight the need to identify alternative si
48 l needs produce motivational drives, such as thirst and hunger, that regulate behaviors essential to
52 onstrate a pivotal role in the regulation of thirst and salt appetite of angiotensin II generated in
53 eostatic and behavioral responses associated thirst and salt appetite, although clearly it may relate
54 mation is integrated in the brain to produce thirst and salt appetite; and how these motivational dri
56 thought to be responsible for the increased thirst and sodium appetite caused by hypovolaemia, produ
57 use the physiological mechanisms controlling thirst and sodium appetite continued functioning without
65 hanges in extracellular osmolarity stimulate thirst and vasopressin secretion through a central osmor
68 hat play key roles in the central control of thirst and water homeostasis, but the extent to which th
69 pants while they imagined a state of intense thirst and while they imagined drinking to satiate thirs
70 ulosum lamina terminalis (OVLT; which drives thirst) and attenuates that of neurosecretory neurons in
71 be pursued (e.g., when balancing hunger and thirst) and how to combine these signals with estimates
73 and physiological variables, such as hunger, thirst, and effort levels, by orchestrating sensory, pro
75 nsin II (AngII)-regulated behaviors, such as thirst, and may do so by influencing the central renin-a
78 aditionally used to treat cholera, alleviate thirst, and serves as an important water source and live
79 by the hormone asprosin, leading to enhanced thirst, and that optogenetic or chemogenetic activation
80 rinking during meals, the rapid satiation of thirst, and the fact that oral cooling is thirst-quenchi
81 ress competing motivational systems, such as thirst, anxiety-related behavior, innate fear, and socia
85 during the appetitive phase, both hunger and thirst are sensed by a nearly identical population of in
92 pacity, loss of or change in smell or taste, thirst, chronic cough, chest pain, and abnormal movement
93 ess, palpitations, change in smell or taste, thirst, chronic cough, chest pain, shortness of breath,
98 irst were significantly higher for imagining thirst compared with imagining drinking or baseline, rev
106 relationship between fatigue, pruritus, and thirst distress (TD) with QOL of patients receiving hemo
108 tion form, the Fatigue Assessment Scale, the Thirst Distress Scale, the Pruritus Severity Scale, the
111 dependently, interactions between hunger and thirst drives are important to coordinate competing need
112 stinct neural circuits underlying hunger and thirst drives in the adult brain have been characterized
117 lated to vegetative and affective aspects of thirst experiences, whereas activity in neocerebellar (p
118 ts attributed to tolvaptan were pollakiuria, thirst, fatigue, dry mouth, polydipsia, and polyuria.
119 cemia, such as frequent urination, increased thirst, fatigue, or visual changes, and had no known fam
121 in humans that drinking water in response to thirst following fluid loss is a pleasant experience.
125 However, continuing to drink water once thirst has been satiated becomes unpleasant and, eventua
127 While central neural circuits regulating thirst have been well studied, it is still unclear how m
129 c mice display high blood pressure, enhanced thirst, high urine output, proteinuria, and kidney damag
131 rnal state of an individual-as it relates to thirst, hunger, fear, or reproductive drive-can be infer
132 vegetative systems including hunger for air, thirst, hunger, pain, micturition, and sleep, is discuss
135 Thus, neural representations of hunger and thirst in mice become distinct before food- and water-se
137 gly, while artificial induction of hunger or thirst in sated mice via activation of specific hypothal
139 the loss of body fluid induces hypovolaemic thirst, in which animals seek both water and minerals (s
140 n previous studies of physiologically evoked thirst, including the anterior midcingulate cortex (aMCC
147 how the neural representation of subjective thirst is generated and how it subsequently motivates dr
149 ysiological drives, such as hunger, sex, and thirst, it is less obvious what drives us to sleep and w
150 o cognitive function, dyspnea, constipation, thirst, leg swelling, numbness, dry mouth, and balance p
153 NA species, whereas a behavior as complex as thirst may be influenced by changes in multiple genes.
154 influence of motivational state (hunger and thirst), memory demand, and spatial behavior in 2 tasks:
157 Furthermore, optogenetic gain of function in thirst-modality-specific cell types recapitulated water-
158 Our results show that the cerebellum is a thirst-modulating brain area and that asprosin-Ptprd sig
160 m ~24,000 neurons in 34 brain regions during thirst-motivated choice behavior in 21 mice as they cons
163 contains NaCl-sensitive neurons to regulate thirst, neuroendocrine function, and autonomic outflow.
171 response to overnight fluid deprivation, or thirst or salt appetite in response to an isotonic hypov
173 minating Agt from hepatocytes did not reduce thirst or sodium appetite, and in fact, these mice consu
180 rimination cued by internal state (hunger or thirst) or on performance of conditional visuospatial ob
183 pparently not involved in the computation of thirst per se but rather is activated during changes in
184 ients and an additional 15 matched controls, thirst perception and neuronal activity in response to b
187 ng deep-brain calcium dynamics, we show that thirst-promoting SFO neurons respond to inputs from the
190 Here, we show that hypothalamic hunger and thirst regions already exhibit specific responses to sta
192 nervous system (CNS), including promotion of thirst, regulation of vasopressin secretion, and modulat
193 lumn, orofacial motor-related, humorosensory/thirst-related, brainstem autonomic control network, neu
194 connectivity with the insula during imagined thirst relative to imagined drinking, implying functiona
196 ntial homeostatic processes, such as hunger, thirst, reproduction and immune responses(1)(,)(2)(,)(3)
203 re, we identified neural circuits underlying thirst satiation and examined their contribution to rewa
205 fast dopamine (DA) sensor to examine whether thirst satiation itself stimulates the reward-related ci
206 Importantly, chemogenetic stimulation of thirst satiation neurons did not activate DA neurons und
208 se but rather is activated during changes in thirst/satiation state when the brain is "vigilant" and
209 focal optogenetic activation of hypothalamic thirst-sensing neurons returned global activity to the p
210 erebral blood flow with subjects' ratings of thirst showed major activation in the vermal central lob
212 urons (ISNs) respond to intrinsic hunger and thirst signals to oppositely regulate sucrose and water
213 w dopamine signals associated with quenching thirst, singing a good song and courting a mate change a
214 ating dopaminergic neurons (DANs) to promote thirst-specific water memory expression, whereas it acti
215 odal physiological state, and that different thirst states are mediated by specific neuron types in t
216 decisions, we found that varying hunger and thirst states caused need-inappropriate choices, such as
217 across sexes, and how inter-drinking session thirst states predict future alcohol intakes in females,
219 enetic inhibition of OVLT neurons attenuated thirst stimulated by hypernatremia or elevated AngII but
223 atal regions that respond to both hunger and thirst, subpopulations of neurons respond distinctly to
224 standing of internal osmolyte regulation and thirst suppression could translate to advancements in hu
226 provide a detailed anatomy and physiology of thirst, taste for water, and arginine-vasopressin (AVP)
229 VGLUT2) neurons are a hub between hunger and thirst that specifically controls motivation for food an
230 sleep disturbance, or unsatisfied hunger or thirst that they rated as moderate or severe, whereas de
232 atients seems to be due to an abnormally low thirst threshold, a condition termed dipsogenic DI.
233 ingestion, which promotes acute satiation of thirst through the subfornical organ and other downstrea
235 sent distinct cellular processes to regulate thirst, vasopressin secretion and autonomic function.
240 tate during random foraging, when hunger and thirst were incidental to behavior, and signals derived
243 y weakness, frequent urination and excessive thirst when diagnosed of diabetes mellitus and later exp
245 n, possibly reflecting anticipatory prandial thirst, with again no influence on the amount of fluid c
246 -OH-DPAT-induced 5-HT hypofunction increases thirst without substantially affecting the palatability