Rapid effect of change in cerebrospinal fluid sodium concentration on salt appetite

Weisinger, R. S.; Considine, P. J.; Denton, Derek A.; McKinley, MJ; Mouw, David R.

doi:10.1038/280490a0

Cited by 49 publications

(37 citation statements)

References 14 publications

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“…Intraventricular injection of CSF [Na + , 500 mM] rapidly decreased deprivation-induced sodium intake in sheep (Weisinger et al, 1979). However, when osmolality of the CSF was increased by intraventricular injection of mannitol, which decreased [Na + ], sodium intake was augmented (Weisinger et al, 1979). These results suggest that the brain contains sodium-sensitive neurons or osmoreceptors that monitor the [Na + ] of CSF and regulate the ingestion of sodium accordingly.…”

Section: Other Contributors : Baroreceptors and Osmoreceptorsmentioning

confidence: 99%

“…Support for osmoreceptor regulation of salt appetite comes from studies that manipulated the sodium concentration of CSF and subsequently examined sodium consumption. Intraventricular injection of CSF [Na + , 500 mM] rapidly decreased deprivation-induced sodium intake in sheep (Weisinger et al, 1979). However, when osmolality of the CSF was increased by intraventricular injection of mannitol, which decreased [Na + ], sodium intake was augmented (Weisinger et al, 1979).…”

Section: Other Contributors : Baroreceptors and Osmoreceptorsmentioning

confidence: 99%

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Richter and sodium appetite: From adrenalectomy to molecular biology

Krause

Sakai

2007

Appetite

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Nearly three-quarters of a century ago, Curt Richter removed the adrenal glands from rats and noted that the animal's vitality was dependent on its increased consumption of sodium chloride. In doing so, Richter revealed an innate behavioral mechanism that serves to maintain the hydromineral balance of an animal faced with sodium deficit. This experiment and others like it, led to the development of a field of research devoted to the investigation of salt appetite. The following is a discussion of how Richter's initial observations gave birth to an evolving field that incorporates multiple approaches to examine the drive to consume sodium. KeywordsSalt appetite; Angiotensin; Aldosterone; Corticosterone; Richter The Discovery of Salt AppetiteAt the time that Richter began his career at Johns Hopkins University much of the research examining ingestive behavior focused on the responses of individual organs or closely coordinated systems. Richter's pioneering work initiated a fundamental paradigm shift that moved the focus to adaptations of the organism as a whole. Specifically, he was interested in changes in behavior that compensated for perturbations in the internal environment. His approach toward investigation of such behaviors was as thorough as it was fundamental. Richter manipulated diet, interfered with the nervous system, and removed or replaced glandular secretions in attempt to understand the nutritional, neural, and endocrine signals that contribute to behavior.Richter created disturbances in the nutritional or mineral content of the internal environment with dietary deficiency. Subsequently, "self selection" experiments were performed where choices of different minerals and nutrients were presented for consumption. More often than not, animals would consume minerals and nutrients in amounts that would alleviate their experimentally-induced deficiencies. One of the most striking behaviors that Richter observed was that of rats voluntarily ingesting salt when faced with sodium deficit. Sodium chloride was removed from the rats' food and they were given access to water and 3 % NaCl solution. The intake of the NaCl solution was approximately 1% of the total diet, which remarkably, is the

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Section: Other Contributors : Baroreceptors and Osmoreceptorsmentioning

confidence: 99%

Section: Other Contributors : Baroreceptors and Osmoreceptorsmentioning

confidence: 99%

Richter and sodium appetite: From adrenalectomy to molecular biology

Krause

Sakai

2007

Appetite

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“…One major challenge in neurobiology of the hydromineral homeostasis is to reveal the existence, at the level of the brain, of specific sensors involved in the control of the water and mineral balance. Fluctuations in plasma and CSF [Na ϩ ] not only trigger short-term adjustments, such as the release of antidiuretic and natriuretic hormones from the neurohypophysis (Bourque et al, 1994;Hussy et al, 2000;Voisin and Bourque, 2002), but also long-term regulation that controls thirst and specific appetite for salt (Weisinger et al, 1979(Weisinger et al, , 1982Denton et al, 1996). It has been hypothesized that specific brain Na ϩ sensors initiate sodium intake (Weisinger et al, 1979;Denton et al, 1996) as well as natriuresis (Cox et al, 1987;Denton et al, 1996), and the recent discovery of coincident detectors of extracellular fluid osmolarity and [Na ϩ ] in the supraoptic nucleus (SON) established the cellular basis for Na ϩ detection in this nucleus (Voisin et al, 1999;Voisin and Bourque, 2002).…”

Section: Introductionmentioning

confidence: 99%

Specific Na⁺Sensors Are Functionally Expressed in a Neuronal Population of the Median Preoptic Nucleus of the Rat

Grob¹,

Drolet²,

Mouginot³

2004

J. Neurosci.

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] out exclusively. The specific Na ϩ response was voltage insensitive and depended on the driving force for Na ϩ ions, indicating that a sustained background Na ϩ permeability controlled the membrane potential of the MnPO neurons. This specific response was not reduced by Gd 3ϩ , amiloride, or benzamil, ruling out the participation of mechanosensitive cationic channels, specific epithelial Na ϩ channels, and Phe-Met-Arg-Phe-gated Na ϩ channels, respectively. Combination of in situ hybridization, using a riboprobe directed against the atypical Na ϩ channel (Na X ), and immunohistochemistry, using an antibody against neuron-specific nuclei protein, revealed that a substantial population of MnPO neurons expressed the Na X channel, which was characterized recently as a concentration-sensitive Na ϩ channel. This study shows that a neuronal population of the MnPO acts as functional Na ϩ sensors and that the Na X channel might represent the molecular basis for the extracellular sodium level sensing in these neurons.

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“…Therefore, there must be two central circuits that are activated by different types of dehydration and inhibited by α 2 -adrenoceptors, one for the control of water and the other for the control of saline intake. As mentioned above, these circuits share the activation by ANG II and by volume receptors during extracellular dehydration (1,15,16), but one (water) is activated (1,28,29) and the other (saline) is inhibited (17,30,31) by the increase in osmolality or in sodium concentration. Furthermore, aldosterone release activated by ANG II during (15), in spite of the controversy on whether central or systemic ANG II is important for saline intake (15,(33)(34)(35)(36).…”

Section: Water Intakementioning

confidence: 99%

Multifactorial control of water and saline intake: role of <FONT FACE=Symbol>a</font>2-adrenoceptors

Deluca¹,

Menani²

1997

Braz J Med Biol Res

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Water and saline intake is controlled by several mechanisms activated during dehydration. Some mechanisms, such as the production of angiotensin II and unloading of cardiovascular receptors, activate both behaviors, while others, such as the increase in blood osmolality or sodium concentration, activate water, but inhibit saline intake. Aldosterone probably activates only saline intake. Clonidine, an α 2 -adrenergic agonist, inhibits water and saline intake induced by these mechanisms. One model to describe the interactions between these multiple mechanisms is a wire-block diagram, where the brain circuit that controls each intake is represented by a summing point of its respective inhibiting and activating factors. The α 2 -adrenoceptors constitute an inhibitory factor common to both summing points.

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Rapid effect of change in cerebrospinal fluid sodium concentration on salt appetite

Cited by 49 publications

References 14 publications

Richter and sodium appetite: From adrenalectomy to molecular biology

Richter and sodium appetite: From adrenalectomy to molecular biology

Specific Na⁺Sensors Are Functionally Expressed in a Neuronal Population of the Median Preoptic Nucleus of the Rat

Multifactorial control of water and saline intake: role of <FONT FACE=Symbol>a</font>2-adrenoceptors

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Rapid effect of change in cerebrospinal fluid sodium concentration on salt appetite

Cited by 49 publications

References 14 publications

Richter and sodium appetite: From adrenalectomy to molecular biology

Richter and sodium appetite: From adrenalectomy to molecular biology

Specific Na+Sensors Are Functionally Expressed in a Neuronal Population of the Median Preoptic Nucleus of the Rat

Multifactorial control of water and saline intake: role of <FONT FACE=Symbol>a</font>2-adrenoceptors

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Specific Na⁺Sensors Are Functionally Expressed in a Neuronal Population of the Median Preoptic Nucleus of the Rat