Regulatory volume decrease and associated osmolyte fluxes in cerebellar granule neurons are calcium independent

Morán, Julio; Morales-Mulia, Sandra; Hernández‐Cruz, Arturo; Pasantes‐Morales, Herminia

doi:10.1002/(sici)1097-4547(19970115)47:2<144::aid-jnr3>3.0.co;2-f

Cited by 41 publications

(16 citation statements)

References 23 publications

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“…Several earlier studies have addressed the cell volume changes induced by anisotonicity and have described volume regulatory mechanisms dependent on or independent of [Ca 2+ ] i [21,25]. Assuming that cells should respond similarly to volume alterations under anisotonic or isotonic conditions, it is not clear why after brain injury and in other pathological states, cells do not regulate their volume.…”

Section: Discussionmentioning

confidence: 99%

Calcium and voltage-dependent alterations of cell volume in neuroblastoma×glioma hybrid NG108-15 cells

Bostel

Malo

Rouzaire‐Dubois

et al. 2002

Pflügers Arch - Eur J Physiol

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Intracellular calcium ([Ca2+](i)), cell volume, membrane potential and currents were measured in neuroblastomaxglioma hybrid cells to gain insight into how [Ca2+](i) controls cell volume. [Ca2+](i) was increased by fluid shear stress, mechanical stimulation of the cells, the Ca2+ ionophore A23187, caffeine and thapsigargin. The increase in [Ca2+](i) induced by mechanical stimulation was decreased by about 50% by caffeine and abolished after incubation of the cells in a Ca2+-free solution. Mechanical stimulation by stirring the cell suspension induced cell shrinkage that was abolished by caffeine, but induced cell swelling in Ca2+-free solution. In the presence of caffeine, A23187 induced cell shrinkage whereas thapsigargin induced cell swelling. Both cell volume changes were inhibited by the Cl- channel blocker 5-nitro-2-(3-phenylpropylamino) benzoic acid. The cells were hyperpolarized by fluid shear stress and A23187 and depolarized by caffeine, thapsigargin and intracellular EGTA. Under all these conditions, the membrane input resistance was decreased. Voltage-clamp experiments suggested that, in addition to an increased anionic current, fluid shear stress and A23187 increased a K+ current, whereas caffeine and intracellular Ca2+ chelation increased a non-selective cation current and thapsigargin increased both a K+ and a non-selective cation current. Taken together, these results suggest that, if cell volume is closely dependent on [Ca2+](i) and the activity of Cl- channels, its relative value is dependent on the ionic selectivity of co-activated channels and the membrane potential.

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Section: Discussionmentioning

confidence: 99%

Calcium and voltage-dependent alterations of cell volume in neuroblastoma×glioma hybrid NG108-15 cells

Bostel

Malo

Rouzaire‐Dubois

et al. 2002

Pflügers Arch - Eur J Physiol

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“…Previously, we and others had demonstrated that increases in [Ca 2ϩ ] i or in PKC activity are not prerequisites for the basal (swelling-induced) release of organic osmolytes such as taurine and D-aspartate from neurotumor cells, neurons, or astrocytes (Moran et al, 1997;Mongin and Kimelberg, 2002;Cardin et al, 2003;Loveday et al, 2003;Cheema et al, 2005). Likewise, in the present study, we observed that, at least under mildly hypotonic conditions, the basal release of 125 I Ϫ also appears to be essentially independent of Ca 2ϩ availability and PKC activity.…”

Section: Discussionmentioning

confidence: 99%

Receptor Regulation of the Volume-Sensitive Efflux of Taurine and Iodide from Human SH-SY5Y Neuroblastoma Cells: Differential Requirements for Ca²⁺ and Protein Kinase C

Cheema

Pettigrew

Fisher

2006

J Pharmacol Exp Ther

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The basal (swelling-induced) and receptor-stimulated effluxes of 125 I Ϫ and taurine have been monitored to determine whether these two osmolytes are released from human SH-SY5Y cells under hypotonic conditions via common or distinct mechanisms. Under basal conditions, both 125 I Ϫ (used as a tracer for Cl Ϫ ) and taurine were released from the cells in a volumedependent manner. The addition of thrombin, mediated via the proteinase-activated receptor-1 (PAR-1) subtype, significantly enhanced the release of both 125 I Ϫ and taurine (3-6-fold) and also increased the threshold osmolarity for efflux of these osmolytes ("set-point") from 200 to 290 mOsM. Inclusion of a variety of broad-spectrum anion channel blockers and of 4-[(2-butyl-6,7-dichloro-2-cyclopentyl-2,3-dihydro-1-oxo-1H-inden-5-yl)oxy]butanoic acid attenuated the release of both 125 I Ϫ and taurine under basal and receptor-stimulated conditions. Basal release of 125 I Ϫ and taurine was independent of Ca 2ϩ or the activity of protein kinase C (PKC). However, although PAR-1-stimulated taurine efflux was attenuated by either a depletion of intracellular Ca 2ϩ or inhibition of PKC by chelerythrine, the enhanced release of 125 I Ϫ was independent of both parameters. Stimulated efflux of 125 I Ϫ after activation of muscarinic cholinergic receptors was also markedly less dependent on Ca 2ϩ availability and PKC activity than that observed for taurine release. These results indicate that, although the osmosensitive release of these two osmolytes from SH-SY5Y cells may occur via pharmacologically similar membrane channels, the receptor-mediated release of 125 I Ϫ and taurine is differentially regulated by PKC activity and Ca 2ϩ availability.Cell volume is constantly subject to change as a consequence of solute accumulation, oxidative metabolism, or fluctuations in the osmolarity of the extracellular fluid. To survive, cells need to regulate their volume within relatively narrow limits, and this homeostatic mechanism is of particular importance to the brain because of the restrictions of the skull. A common cause of brain swelling is hyponatremia, a condition that disproportionately affects the elderly, infants, marathon runners, and military personnel (Upadhyay et al., 2006). Hyponatremia is associated with a variety of neurological symptoms, such as disorientation, mental confusion, and seizures (Kimelberg, 2000;Pasantes-Morales et al., 2000.In response to hypotonic stress, cells swell with a magnitude proportional to the reduction in osmolarity. This is followed by a homeostatic mechanism termed regulatory volume decrease (RVD) that involves the extrusion of intracellular ions such as K ϩ , Cl Ϫ , and a number of organic osmolytes, which together facilitate the loss of water to normalize cell volume (Pasantes-Morales et al., 2000). Inorganic ions constitute two-thirds of the osmolytes released during RVD, and the remainder are accounted for by "compatible" organic osmolytes such as polyols, methylamines, and amino acids. Of these, taurine, an amino acid...

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“…In cerebellar astrocytes and granule neuron cells, changes in [Ca 2+ ] i and RVD are not related; thus, [Ca 2+ ] i is thought to be irrelevant as a transduction signal for RVD [30,31]. In endothelial cells, changes in [Ca 2+ ] i and hypotonicity-induced current are not related and is independent of [Ca 2+ ] i [32].…”

Section: Discussionmentioning

confidence: 99%

Permissive role of calcium on regulatory volume decrease in freshly isolated mouse cholangiocytes

Park

Choi

Siegrist

et al. 2007

Pflugers Arch - Eur J Physiol

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Calcium (Ca2+) pathways are important in cell volume regulation in many cells, but its role in volume regulatory processes in cholangiocytes is unclear. Thus, we have investigated the role of Ca2+ in regulatory volume decrease (RVD) in cholangiocytes using freshly isolated bile duct cell clusters (BDCCs) from normal mouse. No significant increase in [Ca2+]i was observed during RVD, while ionomycin and ATP showed significant increases. Confocal imaging also showed no significant changes in the levels or distributions of intracellular Ca2+ during RVD. Cell volume study by quantitative videomicroscopy indicated that removal and chelation of extracellular Ca2+ by ethylene glycol-bis (beta-aminoethyl ether)-N,N,N-tetraacetic acid (EGTA) or administration of nifedipine did not affect RVD but verapamil significantly inhibited the RVD. Moreover, Ca2+ agonists or inhibitors of Ca2+ release from intracellular stores had no significant effect on RVD. However, 1,2-bis (2-aminophenoxy) ethane-N,N,N'N'-tetraacetic acid-AM (BAPTA-AM) showed significant decreases in [Ca2+]i and significantly inhibited RVD, which was reversed with coadministration of valinomycin, suggesting that BAPTA-AM-induced inhibition is due to potassium conductance or other cellular processes requiring permissive [Ca2+](i. These findings indicate that an increase in [Ca2+]i or extracellular Ca2+ is not required for RVD but Ca2+ has a permissive role in RVD of mouse cholangiocytes.

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Regulatory volume decrease and associated osmolyte fluxes in cerebellar granule neurons are calcium independent

Cited by 41 publications

References 23 publications

Calcium and voltage-dependent alterations of cell volume in neuroblastoma×glioma hybrid NG108-15 cells

Calcium and voltage-dependent alterations of cell volume in neuroblastoma×glioma hybrid NG108-15 cells

Receptor Regulation of the Volume-Sensitive Efflux of Taurine and Iodide from Human SH-SY5Y Neuroblastoma Cells: Differential Requirements for Ca²⁺ and Protein Kinase C

Permissive role of calcium on regulatory volume decrease in freshly isolated mouse cholangiocytes

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Regulatory volume decrease and associated osmolyte fluxes in cerebellar granule neurons are calcium independent

Cited by 41 publications

References 23 publications

Calcium and voltage-dependent alterations of cell volume in neuroblastoma×glioma hybrid NG108-15 cells

Calcium and voltage-dependent alterations of cell volume in neuroblastoma×glioma hybrid NG108-15 cells

Receptor Regulation of the Volume-Sensitive Efflux of Taurine and Iodide from Human SH-SY5Y Neuroblastoma Cells: Differential Requirements for Ca2+ and Protein Kinase C

Permissive role of calcium on regulatory volume decrease in freshly isolated mouse cholangiocytes

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Receptor Regulation of the Volume-Sensitive Efflux of Taurine and Iodide from Human SH-SY5Y Neuroblastoma Cells: Differential Requirements for Ca²⁺ and Protein Kinase C