Continuous measurement of Na concentration in CSF during gastric water infusion in dehydrated rats

Nosé, Hiroshi; Doi, Yutaka; Usui, Setsuo; Kubota, Tetsuaki; Fujimoto, Makoto; Morimoto, T.

doi:10.1152/jappl.1992.73.4.1419

Cited by 24 publications

(10 citation statements)

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“…I.8B; Hiyama et al, 2002). The sensitivity and threshold of Na x channels to the extracellular Na-level is in a range of physiological change: sodium concentrations and plasma osmolarity increase by 5-10% during thirst conditions (Wakerley et al, 1978;Nose et al, 1992).…”

Section: Na X Is Equipped With Molecular Properties For the Na-level mentioning

confidence: 99%

“…Then I examined the neuronal activity of GABAergic neurons in the SFO under the high Na condition. I prepared acute slices containing the SFO from GAD-GFP mice and GAD-GFP/Na x -KO (see Watanabe et al, 2006), because the Na concentration in the plasma increases by 5-10% during dehydration (Wakerley et al, 1978;Nose et al, 1992).…”

Section: Na Activates Gabaergic Neurons In the Sfo By A Na X -Dependementioning

confidence: 99%

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Glial Nax Channels Control Lactate Signaling to Neurons for Brain [Na+] Sensing

Shimizu

Watanabe

Hiyama

et al. 2007

Neuron

173

164

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Sodium (Na) homeostasis is crucial for life, and Na levels in body fluids are constantly monitored in the brain. The subfornical organ (SFO) is the center of the sensing responsible for the control of salt-intake behavior, where Na(x) channels are expressed in specific glial cells as the Na-level sensor. Here, we show direct interaction between Na(x) channels and alpha subunits of Na(+)/K(+)-ATPase, which brings about Na-dependent activation of the metabolic state of the glial cells. The metabolic enhancement leading to extensive lactate production was observed in the SFO of wild-type mice, but not of the Na(x)-knockout mice. Furthermore, lactate, as well as Na, stimulated the activity of GABAergic neurons in the SFO. These results suggest that the information on a physiological increase of the Na level in body fluids sensed by Na(x) in glial cells is transmitted to neurons by lactate as a mediator to regulate neural activities of the SFO.

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Section: Na X Is Equipped With Molecular Properties For the Na-level mentioning

confidence: 99%

Section: Na Activates Gabaergic Neurons In the Sfo By A Na X -Dependementioning

confidence: 99%

Glial Nax Channels Control Lactate Signaling to Neurons for Brain [Na+] Sensing

Shimizu

Watanabe

Hiyama

et al. 2007

Neuron

173

164

View full text Add to dashboard Cite

show abstract

“…Thus, the dynamic regulation of Na and water intake is essential to life. When an animal is dehydrated, the Na concentration in body fluids, and accordingly plasma osmolarity, increases by 5-10% (Wakerley et al, 1978;Nose et al, 1992). A line of experimental evidence indicates that an Na increase in body fluids is detected by a putative Na sensor within the brain that is distinct from the osmosensor (McKinley et al, 1978;Denton et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

The Subfornical Organ is the Primary Locus of Sodium-Level Sensing by Na_xSodium Channels for the Control of Salt-Intake Behavior

Hiyama¹,

Watanabe²,

Okado³

et al. 2004

J. Neurosci.

127

130

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Dehydration causes an increase in the sodium (Na) concentration and osmolarity of body fluid. For Na homeostasis of the body, controls of Na and water intake and excretion are of prime importance. However, the system for sensing the Na level within the brain that is responsible for the control of Na-and water-intake behavior remains to be elucidated. We reported previously that the Na x channel is preferentially expressed in the circumventricular organs (CVOs) in the brain and that Na x knock-out mice ingest saline in excess under dehydrated conditions. Subsequently, we demonstrated that Na x is a Na-level-sensitive Na channel. Here we show that the subfornical organ (SFO) is the principal site for the control of salt-intake behavior, where the Na x channel is the Na-level sensor. Infusion of a hypertonic Na solution into the cerebral ventricle induced extensive water intake and aversion to saline in wild-type animals but not in the knock-out mice. Importantly, the aversion to salt was not induced by the infusion of a hyperosmotic mannitol solution with physiological Na concentration in either genotype of mice. When Na x cDNA was introduced into the brain of the knock-out mice with an adenoviral expression vector, only animals that received a transduction of the Na x gene into the SFO among the CVOs recovered salt-avoiding behavior under dehydrated conditions. These results clearly show that the SFO is the center of the control of salt-intake behavior in the brain, where the Na-level-sensitive Na x channel is involved in sensing the physiological increase in the Na level of body fluids.

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“…I prepared acute slices containing the SFO from GAD-GFP mice and GAD-GFP/Na x -KO (see Watanabe et al, 2006), and recorded the firing activity of the GABAergic neurons bearing the fluorescence of GFP as marker by using patch-clamp techniques in the cell-attached mode under a fluorescence microscope. The GABAergic neurons in the SFO of both wild-type and Na x -KO mice showed spontaneous firing at a similar frequency ( because the Na concentration in the plasma increases by 5-10% during dehydration (Wakerley et al, 1978;Nose et al, 1992).…”

Section: Na Activates Gabaergic Neurons In the Sfo By A Na X -Dependementioning

confidence: 97%

Glial Nax channels control lactate signaling to neurons for brain [Na+] sensing

Shimizu¹,

Hiyama²,

Nagakura³

et al. 2007

Neuroscience Research

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Sodium (Na) homeostasis is crucial for life and Na levels in body fluids are constantly monitored in the brain. The subfornical organ (SFO) is the center of the sensing responsible for the control of Na-intake behavior, where Na x channels are expressed in specific glial cells as the Na-level sensor. Na x channel is a concentration-sensitive Na channel with a threshold value of approximately 150 mM for the extracellular Na ion.The Na x -positive glial cells are sensitive to an increase in the extracellular Na level in the physiological range, indicating that glial cells, not neurons, are the primary site of Na-level sensing. However, the mechanism by which the Na signal sensed by "inexcitable" glial cells is transferred to neurons has remained to be elucidated.To gain insight into the cellular processes involving Na x in glial cells, in this doctor thesis, I started in my study with screening for molecules interacting with Na x using the yeast two-hybrid system with each of the cytoplasmic domains of mouse Na x as bait. Among the positive clones isolated from a mouse DRG cDNA library by using the C-terminal region of Na x as bait, three clones coded for the α subunit of Coexpression of the α1 subunit of Na + /K + -ATPase and Na x channels was examined by double-fluorescent immunostaining using sections of the SFO and dissociated cells from the SFO. The α1 subunit was broadly distributed throughout the iii SFO, overlapping with the expression of Na x channels. The confocal microscopic analyses with isolated cells from the SFO showed that both molecules were colocalized in the plasma membrane. Na x channels were expressed in large round cells, but not in small cells with neurite-like processes, indicating that Na x channels are expressed in glial cells including ependymal cells.It is known that the α2 and α3 isoforms of Na + /K + -ATPase are also expressed in the brain. Experiments using the yeast two-hybrid system showed that the cytoplasmic fragment of α2 corresponding to the region of the α1 isoform isolated also interacted with the C-terminal region of Na x , but that of α3 did not. Thus, Na x has specific interaction with α1 and α2 isoforms of Na and α2 subunits significantly suppressed the metabolic response in the C6M16 cells with Na x expression in the 170 mM Na solution. In contrast, overexpression of the fragment of the α3 subunit, which was negative for interaction with Na x channel, did not affect the metabolic activation.The C-terminal fragment of Na x was also expected to work as a competitor for the binding of Na x channels to Na + /K + -ATPase. Unexpectedly but intriguingly, overexpression of the C-terminal fragment of Na x further enhanced the 2-NBDG uptake, when it was coexpressed in Na x -positive cells. This suggests that the C-terminal region of Na x is also able to support Na + /K + -ATPase, as well as the native Na x . However, the expression of the C-terminal fragment of Na x by itself (without concomitant expression of the native Na x ) exerted no effect on the 2-NBDG uptake. This ...

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Continuous measurement of Na concentration in CSF during gastric water infusion in dehydrated rats

Cited by 24 publications

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Glial Nax Channels Control Lactate Signaling to Neurons for Brain [Na+] Sensing

Glial Nax Channels Control Lactate Signaling to Neurons for Brain [Na+] Sensing

The Subfornical Organ is the Primary Locus of Sodium-Level Sensing by Na_xSodium Channels for the Control of Salt-Intake Behavior

Glial Nax channels control lactate signaling to neurons for brain [Na+] sensing

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Continuous measurement of Na concentration in CSF during gastric water infusion in dehydrated rats

Cited by 24 publications

References 0 publications

Glial Nax Channels Control Lactate Signaling to Neurons for Brain [Na+] Sensing

Glial Nax Channels Control Lactate Signaling to Neurons for Brain [Na+] Sensing

The Subfornical Organ is the Primary Locus of Sodium-Level Sensing by NaxSodium Channels for the Control of Salt-Intake Behavior

Glial Nax channels control lactate signaling to neurons for brain [Na+] sensing

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The Subfornical Organ is the Primary Locus of Sodium-Level Sensing by Na_xSodium Channels for the Control of Salt-Intake Behavior