The lamina terminalis and its role in fluid and electrolyte homeostasis

Gerstberger, Rüdiger; Mathai, Michael L.; Oldfield, Brian J.; Schmid, Herbert

doi:10.1016/s0967-5868(99)90050-4

Cited by 100 publications

(89 citation statements)

References 121 publications

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“…In the previous studies, the osmotic challenge was always achieved by manipulating [Na ϩ ] out , in either the extracellular solution (Travis and Johnson, 1993) or the extracellular fluid compartment (Honda et al, 1990 (Cox et al, 1987;Park et al, 1989;Denton et al, 1996). We now provide evidence for functional Na ϩ sensors in the MnPO that likely belong to a complex neuronal network of interconnected structures within the lamina terminalis (Honda et al, 1990;Oldfield et al, 1991Oldfield et al, , 1992McKinley et al, 1999;McKinley et al, 2003). This network might function as a central osmoregulatory unit that might control vasopressin and may be oxytocin secretion, together with the innate Na ϩ and osmolarity sensitivity of magnocellular neurons (MCNs) (Voisin et al, 1999;Voisin and Bourque, 2002).…”

Section: Discussionmentioning

confidence: 60%

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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Section: Discussionmentioning

confidence: 60%

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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“…These osmoreceptors are located in the AV3V, which is made of a thin membrane, the lamina terminalis, comprising the MnPO, SFO and OVLT. These organs lie outside the blood-brain barrier and therefore are in contact with plasma ions and hormones such as atrial natriuretic peptide (ANP) and angiotensin II (9,10). Vasopressin is rapidly released in response to as little as 1% change in plasma osmolality (11).…”

Section: Neurohypophyseal Hormones and The Control Of Sodium And Watementioning

confidence: 99%

Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion

Ventura

Gomes

Reis

et al. 2002

Braz J Med Biol Res

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The central nervous system plays an important role in the control of renal sodium excretion. We present here a brief review of physiologic regulation of hydromineral balance and discuss recent results from our laboratory that focus on the participation of nitrergic, vasopressinergic, and oxytocinergic systems in the regulation of water and sodium excretion under different salt intake and hypertonic blood volume expansion (BVE) conditions. High sodium intake induced a significant increase in nitric oxide synthase (NOS) activity in the medial basal hypothalamus and neural lobe, while a low sodium diet decreased NOS activity in the neural lobe, suggesting that central NOS is involved in the control of sodium balance. An increase in plasma concentrations in vasopressin (AVP), oxytocin (OT), atrial natriuretic peptide (ANP), and nitrate after hypertonic BVE was also demonstrated. The central inhibition of NOS by L-NAME caused a decrease in plasma AVP and no change in plasma OT or ANP levels after BVE. These data indicate that the increase in AVP release after hypertonic BVE depends on nitric oxide production. In contrast, the pattern of OT secretion was similar to that of ANP secretion, supporting the view that OT is a neuromodulator of ANP secretion during hypertonic BVE. Thus, neurohypophyseal hormones and ANP are secreted under hypertonic BVE in order to correct the changes induced in blood volume and osmolality, and the secretion of AVP in this particular situation depends on NOS activity. Central nervous system and hydromineral balancePrecise regulation of body fluid osmolality is essential. Osmolality is controlled by a finely tuned, intricate homeostatic mechanism that operates by adjusting both the rate of water intake and excretion. The central nervous system (CNS) plays an important role in the control of renal sodium excretion (1-7). Considerable evidence indicates that the median preoptic area (MnPO), anterior lateral hypothalamus, subfornical organ (SFO), anterior portion of the third ventricle (AV3V), supraoptic nucleus (SON), paraventricular nucleus (PVN), organum vasculosum laminae terminalis (OVLT), habenula, stria medullaris, and medial septal area are organized in a neural circuit involved in the regulation of water and sodium intake and excretion (1-3). Natriuresis accompanied by kaliuresis is induced by cholinergic or adrenergic stimulation of the medial septal area, MnPO, anterior lateral hypothalamus, SFO, and AV3V (1,4). Stimulation of AV3V with carbachol, a cholinergic drug, angiotensin II or hypertonic saline enhances natriuresis, which is blocked by the destruction of this brain area (1,4-7). Neurohypophyseal hormones and the control of sodium and water excretionAlthough the neuroendocrine control of sodium and water balance is not completely understood, alterations in volume and osmolality are responsible, at least in part, for changes in plasma vasopressin (AVP) concentration. Verney (8) originally demonstrated that AVP release into the blood is stimulated by the activation of os...

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“…Appropriate regulation of these responses depends on specialized osmosensory neurons that transduce osmotic stimuli into electrical signals that can ultimately modulate homeostatic effector neurons via synaptic contacts. Although osmoresponsive neurons are found in many parts of the CNS (Bourque et al, 1994), previous studies have established that the primary homeostatic osmosensor of the brain is located in the organum vasculosum of the lamina terminalis (OVLT) (Johnson and Gross, 1993;McKinley et al, 1999), a circumventricular organ located at the rostral ventral border of the third ventricle. Lesions encompassing the OVLT abolish the osmotic control of thirst (Buggy and Johnson, 1977;Bealer et al, 1979;McKinley et al, 1982) and vasopressin release from the neurohypophysis (Sladek and Johnson, 1983;Thrasher and Keil, 1987), whereas local osmotic stimulation of the area of the OVLT elicits osmoregulatory responses in water-replete animals (Andersson, 1971;Buggy et al, 1979).…”

Section: Introductionmentioning

confidence: 99%

Transient Receptor Potential Vanilloid 1 Is Required for Intrinsic Osmoreception in Organum Vasculosum Lamina Terminalis Neurons and for Normal Thirst Responses to Systemic Hyperosmolality

Ciura¹,

Bourque²

2006

J. Neurosci.

236

255

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Recent studies have indicated that members of the transient receptor potential vanilloid (TRPV) family of cation channels are required for the generation of normal osmoregulatory responses, yet the mechanism of osmosensory transduction in primary osmoreceptor neurons of the CNS remains to be defined. Indeed, despite ample evidence suggesting that the organum vasculosum lamina terminalis (OVLT) serves as the primary locus of the brain for the detection of osmotic stimuli, evidence that neurons in the OVLT are intrinsically osmosensitive has remained elusive. Here we show that murine OVLT neurons are intrinsically sensitive to increases in the osmolality of the extracellular fluid. Hypertonic conditions provoked increases in membrane cation conductance that resulted in the generation of an inward current, depolarizing osmoreceptor potentials, and enhanced action potential discharge. Moreover, we found that this osmosensory signal transduction cascade was absent in OVLT neurons from TRPV1 knock-out (TRPV1 Ϫ/Ϫ ) mice and that responses of wild type (WT) OVLT neurons could be blocked by ruthenium red, an inhibitor of TRPV channels. Finally, TRPV1 Ϫ/Ϫ mice showed significantly attenuated water intake in response to systemic hypertonicity compared with WT controls. These findings indicate that OVLT neurons act as primary osmoreceptors and that a product of the trpv1 gene is required for osmosensory transduction.

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The lamina terminalis and its role in fluid and electrolyte homeostasis

Cited by 100 publications

References 121 publications

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

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

Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion

Transient Receptor Potential Vanilloid 1 Is Required for Intrinsic Osmoreception in Organum Vasculosum Lamina Terminalis Neurons and for Normal Thirst Responses to Systemic Hyperosmolality

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The lamina terminalis and its role in fluid and electrolyte homeostasis

Cited by 100 publications

References 121 publications

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

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

Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion

Transient Receptor Potential Vanilloid 1 Is Required for Intrinsic Osmoreception in Organum Vasculosum Lamina Terminalis Neurons and for Normal Thirst Responses to Systemic Hyperosmolality

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

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