Potassium and Taurine Release Are Highly Correlated with Regulatory Volume Decrease in Neonatal Primary Rat Astrocyte Cultures

Vitarella, Domenico; DiRisio, Darryl J.; Kimelberg, Harold K.; Aschner, Michael

doi:10.1046/j.1471-4159.1994.63031143.x

Cited by 122 publications

(43 citation statements)

References 28 publications

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“…In the current study, the characteristics of OTR were found to be similar to other studies using C6 glioma cells and astrocytes, in terms of increase in OTR rate following hypoosmotic exposure and the time taken to reach the maximal taurine release rate [43,44]. Furthermore, OTR in the current study demonstrated a similar pharmacological profile to that exhibited by other neuronal cells: the anion channel blockers NPPB (100 lM) and DIDS (100 lM) decreased the OTR rate by approximately the same percentage as previously observed in astrocytes [45].…”

Section: Anion Channel Blockers Decrease the Otr Ratesupporting

confidence: 86%

Inhibition of ERK and JNK Decreases Both Osmosensitive Taurine Release and Cell Proliferation in Glioma Cells

et al. 2007

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Cell swelling is associated with the activation of an increase in the osmosensitive taurine release (OTR) rate, which serves to decrease cell volume as part of a process known as regulatory volume decrease. OTR, which is sensitive to many pharmacological agents including anion channel blockers and signalling pathway modulators, has also been suggested to play a role in cell cycle progression. At non-cytotoxic concentrations, the anion channel blocker NPPB (25 microM), the extra-cellular signal-regulated kinase inhibitor PD98059 (50 microM), and the c-Jun NH2-terminal kinase inhibitor SP 600125 (5 microM) each decreased the OTR rate by > or =50%, decreased cell proliferation, and increased G0/G1 cell cycle arrest.

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Section: Anion Channel Blockers Decrease the Otr Ratesupporting

confidence: 86%

Inhibition of ERK and JNK Decreases Both Osmosensitive Taurine Release and Cell Proliferation in Glioma Cells

et al. 2007

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“…In some cell types, activation of swelling-induced taurine efflux requires extracellular Ca 2ϩ (514,1036), whereas in others, it occurs (674, 733), or is even improved (435,498), in the absence of extracellular Ca 2ϩ (see also sect. VB).…”

Section: Mechanisms Of Activation Of the Taurine Efflux Pathwaymentioning

confidence: 99%

Physiology of Cell Volume Regulation in Vertebrates

Hoffmann

Lambert²,

Pedersen³

2009

Physiological Reviews

1,307

1,677

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The ability to control cell volume is pivotal for cell function. Cell volume perturbation elicits a wide array of signaling events, leading to protective (e.g., cytoskeletal rearrangement) and adaptive (e.g., altered expression of osmolyte transporters and heat shock proteins) measures and, in most cases, activation of volume regulatory osmolyte transport. After acute swelling, cell volume is regulated by the process of regulatory volume decrease (RVD), which involves the activation of KCl cotransport and of channels mediating K+, Cl−, and taurine efflux. Conversely, after acute shrinkage, cell volume is regulated by the process of regulatory volume increase (RVI), which is mediated primarily by Na+/H+exchange, Na+-K+-2Cl−cotransport, and Na+channels. Here, we review in detail the current knowledge regarding the molecular identity of these transport pathways and their regulation by, e.g., membrane deformation, ionic strength, Ca2+, protein kinases and phosphatases, cytoskeletal elements, GTP binding proteins, lipid mediators, and reactive oxygen species, upon changes in cell volume. We also discuss the nature of the upstream elements in volume sensing in vertebrate organisms. Importantly, cell volume impacts on a wide array of physiological processes, including transepithelial transport; cell migration, proliferation, and death; and changes in cell volume function as specific signals regulating these processes. A discussion of this issue concludes the review.

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“…Swelling of the end feet of astrocytic perivascular processes may also lead to altered cerebral blood flow [71]. Cell swelling is rapidly followed by regulatory volume decrease and the release of organic osmolytes, of which the amino acid taurine is of especial interest [72][73][74][75]. Taurine has previously been shown to increase accumbal dopamine levels, and appears to be a key component in ethanol induced dopamine release [76][77][78].…”

Section: Astrocytic Cell Swellingmentioning

confidence: 99%

Astrocyte Function in Alcohol Reward and Addiction

Adermark¹

2015

J Alcohol Drug Depend

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Glial cells, particularly astrocytes, play essential roles in the regulation of neurotransmission, metabolism, and supply of energy substrates for synaptic transmission. One astrocyte can receive inputs from several hundreds of synapses, and synchronized neuronal activity correlates with astrocyte calcium signaling. Astrocyte pathology is a common feature of ethanol exposure in both humans and animal models, and brief alcohol intake is sufficient to cause long-lasting changes in astrocyte gene expression, activity and proliferation. Recent research also suggests that astrocytes shape the rewarding sensation of ethanol, and might be involved in modulating alcohol consumption. Considering the role of astrocytes in regulating glutamate homeostasis, a crucial component of alcohol abuse disorders, the astrocyte might be an important target for the development of new pharmacological treatments of alcoholism.Keywords: Alcohol; Astrocytes; Astroglia; Glia; GFAP; Dopamine; Ethanol AstrocytesThe astroglial cell, or astrocyte, is the most numerous cell type of the glial cell family. Astrocytes give structural and metabolic support to surrounding neurons and are pivotal for neuronal functioning and signal processing in the CNS [1,2] (Figure 1). The end feet of astrocytic processes encapsulate blood vessels and participate in building up the blood brain barrier [3,4]. The contact with blood vessels also enables the astrocytes to provide neurons with lactate under anaerobic conditions [1,5] (Figure 1). The astrocyte was first acknowledged as the primary cell type responsible for potassium buffering [6], and combined with the clearance of amino acids from the extracellular space, astrocytes warrants a high signal to noise ratio, and reduced receptor desensitization [7,8]. One single astrocyte can enwrap several neuronal somata and receive inputs from thousands of synapses, enabling them to sense and integrate synaptic activity [9,10]. Activation of astrocytes also appears to be a crucial component for the induction of synaptic plasticity mechanisms, and both long-term potentiation (LTP) and long-term depression (LTD) in the hippocampus may be regulated by astrocytes [11,12].Astrocytes enwrap both presynaptic and postsynaptic terminals, forming the tripartite synapse. Astrocytic end feet encapsulate blood vessels, enabling the astrocyte to give metabolic support to surrounding neurons. Astrocytic clearance of neuroactive substances is crucial for synaptic transmission. The excitatory amino acid glutamate (Glu) is rapidly metabolized to its non-excitable precursor glutamine (Gln), released back to the extracellular space, and taken up by neurons for synthesis of glutamate or GABA. See text for further details. Astrocytic transportersOne of the most prominent functions of the astrocyte is the clearance of glutamate, and astrocytic glutamate transporters EAAT2 (GLT-1) and EAAT1 (GLAST) are the most abundant transporters for removal of glutamate in the brain [13]. Impaired astrocytic glutamate clearance appears to contribut...

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Potassium and Taurine Release Are Highly Correlated with Regulatory Volume Decrease in Neonatal Primary Rat Astrocyte Cultures

Cited by 122 publications

References 28 publications

Inhibition of ERK and JNK Decreases Both Osmosensitive Taurine Release and Cell Proliferation in Glioma Cells

Inhibition of ERK and JNK Decreases Both Osmosensitive Taurine Release and Cell Proliferation in Glioma Cells

Physiology of Cell Volume Regulation in Vertebrates

Astrocyte Function in Alcohol Reward and Addiction

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