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How Does the Brain Sense Osmolality?

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How Does the Brain Sense Osmolality? SCIENCE IN RENAL MEDICINE www.jasn.org How Does the Brain Sense Osmolality? Joseph G. Verbalis Professor of Medicine and Physiology, Georgetown University School of Medicine, Washington, DC ABSTRACT For nearly 60 years, we have known that the brain plays a pivotal role in regulating sponses to hyperosmolality in experi- the osmolality of body fluids. Over this time period, scientists have determined the mental animals3 and in human subjects structure and function of arginine vasopressin and its receptors, the role of the with brain damage that infarcts the re- posterior pituitary as a storage site, and the determinants of vasopressin release. gion around the OVLT, who typically are The cellular mechanisms by which the kidney responds to vasopressin are also well unable to maintain normal plasma os- understood. One area that remains unclear is the neural mechanisms underlying molalities even under basal conditions.4 osmoreception. New findings have implicated the TRPV family of cation channels as In contrast to the effects of such lesions osmo-mechanoreceptors that may mediate the neuronal responses to changes in to eliminate both osmotically stimulated systemic tonicity. This topic is reviewed here. thirst and AVP secretion, diabetes insip- idus caused by destruction of the magno- J Am Soc Nephrol 18: 3056–3059, 2007. doi: 10.1681/ASN.2007070825 cellular AVP neurons in the supraoptic (SON) and paraventricular (PVN) nu- clei eliminates dehydration-induced Body fluid homeostasis is directed at WHERE ARE OSMORECEPTORS AVP secretion but not thirst, clearly in- maintaining the stability of the osmo- LOCATED? dicating that osmotically stimulated lality of body fluids (osmotic ho- thirst must be generated proximally to meostasis) and the intravascular blood The pioneering investigations of Verney the AVP-secreting cells themselves (Fig- volume (volume homeostasis). Os- in the 1940s1 found infusion of hyperos- ure 1A). Other regions have also been re- motic regulation serves to minimize motic solutions into blood vessels that ported to contain putative osmorecep- osmotically induced perturbations in perfused the anterior hypothalamus pro- tors, including the hepatic portal cell volume, which has adverse effects duced an antidiuresis in dogs, thereby circulation, leading to the suggestion on multiple cellular functions. Body identifying this area as the site of osmo- that osmoreceptors are widely distribut- fluid osmolality in humans is main- responsive elements in the brain. The ed.5 However, cells in these areas likely tained between 280 and 295 mOsm/kg most parsimonious explanation for these act to modulate the activity of the pri- H2O, representing one of the most findings would be that the AVP-secret- mary OVLT osmoreceptors because they highly regulated parameters of body ing magnocellular neurons themselves are not able to maintain osmotically physiology. This is accomplished are the osmoreceptors. Although these stimulated AVP secretion or thirst after through an integration of thirst, argi- neurons do display osmoreceptive char- lesions of the OVLT. nine vasopressin (AVP) secretion, and acteristics,2 their location inside the Involvement of the OVLT and sur- renal responsiveness to AVP. To pre- blood–brain barrier does not position rounding areas of the anterior hypothal- serve plasma osmolality within such them to respond quickly to small amus in osmoreception is also supported narrow tolerances, pituitary AVP se- changes in osmolality in the circulation. by studies using immunohistochemical cretion must vary in response to small Subsequent studies strongly implicated changes in plasma osmolality, which is the circumventricular organ named the Published online ahead of print. Publication date achieved through the activation or in- organum vasculosum of the lamina ter- available at www.jasn.org. hibition of central osmoreceptor cells. minalis (OVLT), which lacks a blood– Correspondence: Dr. Joseph G. Verbalis, Division Understanding where and how the brain barrier, as well as areas of the adja- of Endocrinology and Metabolism, 232 Building D, brain senses the osmolality of body flu- cent hypothalamus near the anterior wall Georgetown University Medical Center, 3800 Res- ids and transduces this information of the third cerebral ventricle as the site ervoir Road NW, Washington, DC 20007. Phone: 202-687-2818; Fax: 202-444-7797; E-mail: verbalis@ into mechanisms that regulate AVP se- of the principle brain osmoreceptors. georgetown.edu cretion and thirst is the subject of this Destruction of this area of the brain abol- Copyright © 2007 by the American Society of commentary. ishes both AVP secretion and thirst re- Nephrology 3056 ISSN : 1046-6673/1812-3056 J Am Soc Nephrol 18: 3056–3059, 2007 www.jasn.org SCIENCE IN RENAL MEDICINE secretion and thirst, this has not been de- 10 A + Na THIRST finitively confirmed. Separate but paral- 9 sodium chloride Na+ Primary osmo- lel pathways for these complementary + receptors 8 Na functions remain possible (Figure 1B) mannitol Na+ AVP and could account for the lower osmotic 7 threshold for activation of AVP secretion 6 B Primary Na+ 8 thirst compared with thirst. 5 osmo- THIRST + receptor urea Na (pg/mL) 4 + Na Primary AVP Plasma Vasopressin 3 Na+ osmo- AVP WHAT DO BRAIN receptor OSMORECEPTORS RESPOND TO? 2 Figure 1. Brain osmoreceptor pathways. 1 glucose The primary brain osmoreceptors lie out- Neither AVP secretion nor thirst is 0 side the blood–brain barrier in the OVLT. equally sensitive to all plasma solutes. So- 285 295 305 315 Different neural projections connect the dium and its anions, which normally Plasma Osmolality primary osmoreceptors to brain areas re- contribute Ͼ95% of the osmotic pres- (mOsm/kg H2O) sponsible for AVP secretion and thirst. sure of plasma, are the most potent sol- Figure 2. Solute specificity of brain osmo- Whether the same (A) or different subsets utes in terms of their capacity to stimu- receptors. The lines represent the relation- (B) of osmoreceptors project to both areas late AVP secretion and thirst, although ship of plasma AVP to plasma osmolality in is presently unknown. Although osmore- some sugars such as mannitol and su- healthy adults during intravenous infusion ceptors can both stimulate as well as in- crose are also equally effective when in- of hypertonic solutions of different solutes. hibit AVP secretion and thirst in response fused intravenously.8 In contrast, in- Note that effective solutes, i.e., those com- to systemic hyper-and hypotonicity, re- partmentalized to the extracellular fluid spectively, it is also not known whether creases in plasma osmolality caused by (NaCl and mannitol), are much more effec- there are separate subsets of excitatory solutes such as urea or glucose cause little tive at eliciting AVP secretion than the non- and inhibitory osmoreceptor cells, or or no increase in plasma AVP levels in effective solutes, urea and glucose, that whether this is a property of single osmo- humans or animals (Figure 2).8,9 These distribute across cell membranes into the receptive cells. differences in response to various plasma intracellular fluid as well (adapted from solutes are independent of any recog- Zerbe and Robertson GL.8) nized nonosmotic influence, which indi- techniques to detect early gene products cates they are an intrinsic property of the in rats, which serve as markers of cell ac- osmoregulatory mechanism itself. Thus, sensitive neurons has been found to acti- tivation after dehydration. Intense ex- it is clear that osmoreceptor cells in the vate membrane nonselective cationic pression of the cFos protein in and brain primarily respond to plasma tonic- conductances that generate inward cur- around the OVLT confirms this area is ity rather than to total plasma osmolality. rent; if of sufficient magnitude, the re- strongly activated by induced dehydra- The physiological relevance of this find- sulting depolarization of the osmorecep- tion, and retrograde tracing studies ver- ing is that osmoreceptors function pri- tor neuron then produces an action ify that a subset of the activated neurons marily to preserve cell volume; elevations potential.10 Conversely, “ineffective” sol- send projections to the magnocellular of solutes such as urea, unlike elevations utes that penetrate cells readily create no AVP neurons in the hypothalamus.6 Al- of sodium, do not cause cellular dehy- osmotic gradient and thus have little to though many of the neural pathways dration and consequently do not activate no effect on the cell volume of the osmo- connecting the OVLT and other circum- the mechanisms that defend body fluid receptors. Electrophysiological studies of ventricular organs with the magnocellu- homeostasis by preserving or increasing neurons in the OVLT show they display lar AVP-secreting cells in the SON and body water stores. changes in action potential firing rate PVN have been identified, the neural cir- that vary in proportion to the tonicity of cuits in the forebrain that stimulate thirst extracellular fluid, supporting the likeli- after osmoreceptor activation are still hood that these cells represent osmosen- largely unknown. Recent studies using WHAT ARE THE CELLULAR sory neurons.5 Osmotically evoked functional magnetic resonance imaging MECHANISMS UNDERLYING changes in the firing rate of the OVLT in humans have shown that the anterior OSMORECEPTION? neurons in turn synaptically regulate the cingulate area of the cortex is reliably ac- electrical activity of downstream effector tivated in conjunction with the
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