Regulation of taurine transport in rat hippocampal neurons by hypo‐osmotic swelling

Olson, James E.; Martinho, Eduardo

doi:10.1111/j.1471-4159.2006.03652.x

Cited by 18 publications

(24 citation statements)

References 86 publications

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“…Previous studies have indicated that during episodes of hypoosmotic stress organic osmolyte homeostasis is regulated not only via osmolyte efflux but also at the level of osmolyte reuptake (Olson and Martinho, 2006;Foster et al, 2009). Consistent with this possibility, a major finding from the present study is that mAChR-mediated uptake of Daspartate (and to a lesser extent, basal uptake) is significantly attenuated when SH-SY5Y cells are subjected to hypoosmotic stress.…”

Section: Discussionsupporting

confidence: 79%

Muscarinic Receptor Stimulation of d-Aspartate Uptake into Human SH-SY5Y Neuroblastoma Cells Is Attenuated by Hypoosmolarity

Foster

Heacock

Fisher

2010

J Pharmacol Exp Ther

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In addition to its function as an excitatory neurotransmitter, glutamate plays a major role as an osmolyte within the central nervous system (CNS). Accordingly, mechanisms that regulate glutamate release and uptake are of physiological importance not only during conditions in which cell volume remains constant but also when cells are subjected to hypoosmotic stress. In the present study, the ability of muscarinic cholinergic receptors (mAChRs) to regulate the uptake of glutamate (monitored as D-aspartate) into human SH-SY5Y neuroblastoma cells under isotonic or hypotonic conditions has been examined. In isotonic media, agonist activation of mAChRs resulted in a significant increase (250 -300% of control) in the uptake of D-aspartate and, concurrently, a cellular redistribution of the excitatory amino acid transporter 3 (EAAT3) to the plasma membrane. mAChR-mediated increases in D-aspartate uptake were potently blocked by the EAAT3 inhibitor L-␤-threo-benzylaspartate. In hypotonic media, the ability of mAChR activation to facilitate D-aspartate uptake was significantly attenuated (40 -50%), and the cellular distribution of EAAT3 was disrupted. Reduction of mAChR-stimulated D-aspartate uptake under hypoosmotic conditions could be fully reversed upon re-exposure of the cells to isotonic media. Under both isotonic and hypotonic conditions, mAChR-mediated increases in D-aspartate uptake depended on cytoskeletal integrity, protein kinase C and phosphatidylinositol 3-kinase activities, and the availability of intracellular Ca 2ϩ . In contrast, dependence on extracellular Ca 2ϩ was observed only under isotonic conditions. The results suggest that, although the uptake of D-aspartate into SH-SY5Y cells is enhanced after mAChR activation, this process is markedly attenuated by hypoosmolarity.

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Section: Discussionsupporting

confidence: 79%

Muscarinic Receptor Stimulation of d-Aspartate Uptake into Human SH-SY5Y Neuroblastoma Cells Is Attenuated by Hypoosmolarity

Foster

Heacock

Fisher

2010

J Pharmacol Exp Ther

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“…Second, the lack of change in the net content of amino acids other than taurine and alanine may be a result of rapid reuptake into adjacent glial cells or into the neurons from which they were released. Although taurine also is known to be accumulated by neurons and glial cells (6,32,33,71), we found that ATP did not alter unidirectional uptake of taurine into the neuron cultures. Conversely, the broadly acting P2 receptor antagonist suramin increased the rate of taurine accumulation.…”

Section: Discussioncontrasting

confidence: 55%

“…With our methods, these primary cultures of rat hippocampal neurons contained ϳ20% astroglial cells as defined by counts of glial fibrillary acidic protein (GFAP)-positive cells and the specific activity of the astrocyte-specific enzyme glutamine synthetase (71). All cells used in these studies were neurons as defined by their general morphological appearance and the presence of inward currents observed upon membrane depolarization; however, the specific neuronal cell type was not characterized.…”

Section: Discussionmentioning

confidence: 99%

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Purinergic activation of anion conductance and osmolyte efflux in cultured rat hippocampal neurons

Li¹,

Olson²

2008

American Journal of Physiology-Cell Physiology

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Li G, Olson JE. Purinergic activation of anion conductance and osmolyte efflux in cultured rat hippocampal neurons. Am J Physiol Cell Physiol 295: C1550 -C1560, 2008. First published October 15, 2008 doi:10.1152/ajpcell.90605.2007.-The majority of mammalian cells demonstrate regulatory volume decrease (RVD) following swelling caused by hyposmotic exposure. A critical signal initiating RVD is activation of nucleotide receptors by ATP. Elevated extracellular ATP in response to cytotoxic cell swelling during pathological conditions also may initiate loss of taurine and other intracellular osmolytes via anion channels. This study characterizes neuronal ATPactivated anion current and explores its role in net loss of amino acid osmolytes. To isolate anion currents, we used CsCl as the major electrolyte in patch electrode and bath solutions and blocked residual cation currents with NiCl 2 and tetraethylammonium. Anion currents were activated by extracellular ATP with a K m of 70 M and increased over fourfold during several minutes of ATP exposure, reaching a maximum after 9.0 min (SD 4.2). The currents were blocked by inhibitors of nucleotide receptors and volume-regulated anion channels (VRAC). Currents showed outward rectification and inactivation at highly depolarizing membrane potentials, characteristics of swelling-activated anion currents. P2X agonists failed to activate the anion current, and an inhibitor of P2X receptors did not block the effect of ATP. Furthermore, current activation was observed with extracellular ADP and 2-(methylthio)adenosine 5Ј-diphosphate, a P2Y 1 receptor-specific agonist. Much less current activation was observed with extracellular UTP, suggesting the response is mediated predominantly by P2Y 1 receptors. ATP caused a dose-dependent loss of taurine and alanine that could be blocked by inhibitors of VRAC. ATP did not inhibit the taurine uptake transporter. Thus extracellular ATP triggers a loss of intracellular organic osmolytes via activation of anion channels. This mechanism may facilitate neuronal volume homeostasis during cytotoxic edema. amino acids; taurine; cell volume EXTRACELLULAR PURINE AND PYRIMIDINE compounds mediate a variety of brain functions by receptor-mediated action. Extracellular ATP and its metabolic products can initiate cellular responses through two types of receptors: P1 receptors, which are highly sensitive to adenosine, and P2 receptors, sensitive to adenine nucleotides. The P2 receptors are further divided into P2X (ligand-gated channels) or P2Y (G protein-coupled receptors) (1,65,66,77). These receptors are widely distributed in the central nervous system and provoke a variety of effects on neurons and on glial cells.

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“…The taurine transporter (TauT) belongs to the β-amino acid transport system [10][11][12] . This system is specific for taurine and other β-amino acids, such as β-alanine and hypotaurine [13] .…”

mentioning

confidence: 99%

Fluoxetine Treatment in Rats Increases the Rate of Taurine Transport in Mononuclear Cells

Colmenares-Aguilar

Urbina²,

Obregón³

et al. 2017

Neuroimmunomodulation

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Fluoxetine, a selective serotonin reuptake inhibitor antidepressant, modulates the mitogen-induced proliferation of lymphocytes. Lymphocytes contain taurine and express taurine transporter (TauT). Among the effects of taurine on lymphocytes are protection against oxidants and regulation of the inflammatory aspects of the immune response. Our aim was to determine the influence of fluoxetine treatment on taurine transport, and to determine the presence of TauT in the mononuclear cells of rats. Methods: Male adult Sprague-Dawley rats were treated with fluoxetine 10 mg/kg i.p. for 1, 2, and 3 weeks. The cells were obtained by density gradients. [³H]Taurine was used for transport assays. Amino acid levels were determined by high-performance liquid chromatography. Immunolabeling of CD4+, CD8+, and TauT was performed. The mRNA of TauT was evaluated by RT-PCR. Controls were included for each protocol. Results: The transport of taurine, after 1 week of treatment, was significantly augmented compared to controls. The affinity significantly increased at 1 and 2 weeks. While the percentage of CD4+ cells decreased and that of CD8+ cells increased, the percentage of TauT in CD4+ and CD8+ cells was not affected. Reduction of levels of aspartic acid, glutamic acid, threonine, alanine, glycine, and arginine occurred at 1 and 2 weeks. The taurine concentration significantly decreased after 2 and 3 weeks of treatment. The estimation of mRNA of TauT was not different. Conclusion: Taurine transport increases with fluoxetine treatment, and so this could be related to an immunomodulatory role of fluoxetine through TauT. Inhibition of serotonin reuptake might be involved in the regulation of taurine transport in mononuclear cells.

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Regulation of taurine transport in rat hippocampal neurons by hypo‐osmotic swelling

Cited by 18 publications

References 86 publications

Muscarinic Receptor Stimulation of d-Aspartate Uptake into Human SH-SY5Y Neuroblastoma Cells Is Attenuated by Hypoosmolarity

Muscarinic Receptor Stimulation of d-Aspartate Uptake into Human SH-SY5Y Neuroblastoma Cells Is Attenuated by Hypoosmolarity

Purinergic activation of anion conductance and osmolyte efflux in cultured rat hippocampal neurons

Fluoxetine Treatment in Rats Increases the Rate of Taurine Transport in Mononuclear Cells

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