Hyposmolarity-activated fluxes of taurine in astrocytes are mediated by diffusion

Sanchez-Olea, Roberto; Morán, Julio; Schousboe, Arne; Pasantes‐Morales, Herminia

doi:10.1016/0304-3940(91)90404-h

Cited by 103 publications

(45 citation statements)

References 13 publications

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“…Examination of the effects on the Km and V max of this uptake, using initial rates, would likely provide useful information regarding the mecha nism of the inhibition. We and others have sug gested that swelling-induced release of EAA may be due to the opening of swelling-activated channels, which allows anions as large as glutamate to pass (Kimelberg et al, 1990;Sanchez-Olea et al, 1991;Jalonen, 1993;Roy and Malo, 1993). This transport system is also inhibited by anion transport inhibi tors and seems particularly sensitive to the anion transport inhibitor L-644,711, a compound that we have shown is protective in animal models of isch emia and head injury (Cragoe et al, 1986).…”

Section: Discussionmentioning

confidence: 99%

“…Wa ter rapidly enters the cell causing an immediate and maximal swelling which then activates volume reg ulatory processes, principally K + and CI-channels (O'Connor et al, 1993), and possibly a channel as sociated with amino acid efflux because it has many of the characteristics of an anion channel (Sanchez Olea et al, 1991). CI-channels can transport amino acids as well as Cl- (Roy and Malo, 1993).…”

Section: Discussionmentioning

confidence: 99%

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Astrocytic Swelling Due to Hypotonic or High K⁺Medium Causes Inhibition of Glutamate and Aspartate Uptake and Increases Their Release

Kimelberg

Rutledge

Goderie

et al. 1995

J Cereb Blood Flow Metab

158

102

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Summary: Astrocytic swelling occurs readily in ischemia and traumatic brain injury (TBI) as part of the cytotoxic or cellular edema response. Ischemia is known to pro duce large extracellular increases in both [K + 1 and excit atory amino acids (EAA) in vivo, and astrocytic swelling in vitro leads to marked release of EAA. In this study we compared the effect of swelling due to hypotonic media and high K + medium on the uptake and release of EAA by rat primary astrocyte cultures in vitro. In both cases, there was a significant inhibition of uptake of [3HlL glutamate and [3Hln-aspartate, and increased release of preloaded eHln-aspartate. The kinetics of the increased efflux was very different in response to hypotonic or high K + media. In hypotonic medium there was a rapid initial release followed by a decline in the rate of release over time. This release was independent of whether Na + was present. Upon exposure to high K + medium there was a Marked astrocyte swelling is a prominent occur rence during and after ischemia (Ames et aI. , 1968; Garcia et aI. , 1977; Kalimo et aI. , 1977; Jenkins et aI., 1979 Jenkins et aI., , 1982Garcia 1984; Kimelberg and Ran som, 1986;Kraig and Petito, 1989;Hatashita and Hoff, 1990; Chen et aI. , 1992; Siesjo, 1992). In order to study the consequences and mechanisms of such swelling we have used primary astrocyte cultures swollen by hypotonic or high K + solutions as model systems (Walz 1987; O'Connor et ai. , 1992). We and others have observed that exposure to such solu tions will release endogenous or preloaded radiola beled taurine, glutamate, or aspartate, and this ef-

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Astrocytic Swelling Due to Hypotonic or High K⁺Medium Causes Inhibition of Glutamate and Aspartate Uptake and Increases Their Release

Kimelberg

Rutledge

Goderie

et al. 1995

J Cereb Blood Flow Metab

158

102

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“…As mentioned in the Introduction, most animal cells respond to this situation with an active process of volume recovery known as regulatory volume decrease (RVD) (Cala, 1977), which is accomplished by extrusion of the major intracellular ions, K 1 and Cl -, and organic osmolytes. Most of the corrective fluxes occur via K 1 and Cl -channels and diffusion pathways for the organic osmolytes (Hoffmann and Lambert, 1983;Sánchez-Olea et al, 1991;Okada and Maeno, 2001;Hoffmann et al, 2009) (Fig. 1).…”

Section: The Role Of Channels In Regulatory Volume Decreasementioning

confidence: 99%

“…Efflux of organic osmolytes occurs via energy-independent, bidirectional leak pathways with net solute movements driven by the concentration gradient (Hoffmann and Lambert, 1983;Sánchez-Olea et al, 1991). It has been reported consistently that organic osmolyte fluxes are greatly reduced by VRAC blockers, but it is still not known whether Cl -and organic osmolytes permeate across a common pathway, most likely an anion channel like VRAC.…”

mentioning

confidence: 99%

Channels and Volume Changes in the Life and Death of the Cell

Pasantes‐Morales

2016

Mol Pharmacol

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Volume changes deviating from original cell volume represent a major challenge for cellular homeostasis. Cell volume may be altered either by variations in the external osmolarity or by disturbances in the transmembrane ion gradients that generate an osmotic imbalance. Cells respond to anisotonicity-induced volume changes by active regulatory mechanisms that modify the intracellular/extracellular concentrations of K 1 , Cl -, Na 1 , and organic osmolytes in the direction necessary to reestablish the osmotic equilibrium. Corrective osmolyte fluxes permeate across channels that have a relevant role in cell volume regulation. Channels also participate as causal actors in necrotic swelling and apoptotic volume decrease. This is an overview of the types of channels involved in either corrective or pathologic changes in cell volume. The review also underlines the contribution of transient receptor potential (TRP) channels, notably TRPV4, in volume regulation after swelling and describes the role of other TRPs in volume changes linked to apoptosis and necrosis. Lastly we discuss findings showing that multimers derived from LRRC8A (leucine-rich repeat containing 8A) gene are structural components of the volume-regulated Cl -channel (VRAC), and we underline the intriguing possibility that different heteromer combinations comprise channels with different intrinsic properties that allow permeation of the heterogenous group of molecules acting as organic osmolytes.

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“…[12]. Unexpectedly, taurine efflux was found sensitive to Cl -channel blockers [5], and this led to propose an anion channel-like molecule as the transport pathway for Cl -and organic osmolytes [13].…”

Section: Activation and Inactivation Of Corrective Fluxesmentioning

confidence: 99%

Amino Acid Osmolytes in Regulatory Volume Decrease and Isovolumetric Regulation in Brain Cells: Contribution and Mechanisms

Pasantes‐Morales

Franco

Torres-Márquez

et al. 2000

Cell Physiol Biochem

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Brain adaptation to hyposmolarity is accomplished by loss of both electrolytes and organic osmolytes, including amino acids, polyalcohols and methylamines. In brain in vivo, the organic osmolytes account for about 35% of the total solute loss. This review focus on the role of amino acids in cell volume regulation, in conditions of sudden hyposmosis, when cells respond by active regulatory volume decrease (RVD) or after gradual exposure to hyposmotic solutions, a condition where cell volume remains unchanged, named isovolumetric regulation (IVR). The amino acid efflux pathway during RVD is passive and is similar in many respects to the volume-activated anion pathway. The molecular identity of this pathway is still unknown, but the anion exchanger and the phospholemman are good candidates in certain cells. The activation trigger of the osmosensitive amino acid pathway is unclear, but intracellular ionic strength seems to be critically involved. Tyrosine protein kinases markedly influence amino acid efflux during RVD and may play an important role in the transduction signaling cascades for osmosensitive amino acid fluxes. During IVR, amino acids, particularly taurine are promptly released with an efflux threshold markedly lower than that of K⁺, emphasizing their contribution (possibly as well as of other organic osmolytes) vs inorganic ions, in the osmolarity range corresponding to physiopathological conditions. Amino acid efflux also occurs in response to isosmotic swelling as that associated with ischemia or trauma. Characterization of the pathway involved in this type of swelling is hampered by the fact that most osmolyte amino acids are also neuroactive amino acids and may be released in response to stimuli concurrent with swelling, such as depolarization or intracellular Ca⁺⁺ elevation.

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Hyposmolarity-activated fluxes of taurine in astrocytes are mediated by diffusion

Cited by 103 publications

References 13 publications

Astrocytic Swelling Due to Hypotonic or High K⁺Medium Causes Inhibition of Glutamate and Aspartate Uptake and Increases Their Release

Astrocytic Swelling Due to Hypotonic or High K⁺Medium Causes Inhibition of Glutamate and Aspartate Uptake and Increases Their Release

Channels and Volume Changes in the Life and Death of the Cell

Amino Acid Osmolytes in Regulatory Volume Decrease and Isovolumetric Regulation in Brain Cells: Contribution and Mechanisms

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Hyposmolarity-activated fluxes of taurine in astrocytes are mediated by diffusion

Cited by 103 publications

References 13 publications

Astrocytic Swelling Due to Hypotonic or High K+Medium Causes Inhibition of Glutamate and Aspartate Uptake and Increases Their Release

Astrocytic Swelling Due to Hypotonic or High K+Medium Causes Inhibition of Glutamate and Aspartate Uptake and Increases Their Release

Channels and Volume Changes in the Life and Death of the Cell

Amino Acid Osmolytes in Regulatory Volume Decrease and Isovolumetric Regulation in Brain Cells: Contribution and Mechanisms

Contact Info

Product

Resources

About

Astrocytic Swelling Due to Hypotonic or High K⁺Medium Causes Inhibition of Glutamate and Aspartate Uptake and Increases Their Release

Astrocytic Swelling Due to Hypotonic or High K⁺Medium Causes Inhibition of Glutamate and Aspartate Uptake and Increases Their Release