P033. Nitric oxide mediates cytokine-induced enhancement of calcium-dependent glutamate release from astrocytes

Nitric Oxide ◽  
2006 ◽  
Vol 14 (4) ◽  
pp. 29
Author(s):  
Tomoaki Ida ◽  
Shigeru Tsunoda ◽  
Masayuki Hara ◽  
Shunji Kozaki ◽  
Hideshi Ihara
Keyword(s):  
Nitric Oxide ◽  
Glutamate Release ◽  
Calcium Dependent

Cytokine-induced enhancement of calcium-dependent glutamate release from astrocytes mediated by nitric oxide

2008 ◽  
Vol 432 (3) ◽  
pp. 232-236 ◽  
Author(s):  
Tomoaki Ida ◽  
Masayuki Hara ◽  
Yoichi Nakamura ◽  
Shunji Kozaki ◽  
Shigeru Tsunoda ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Glutamate Release ◽  
Calcium Dependent

Mechanisms of inflammatory neurodegeneration: iNOS and NADPH oxidase

2007 ◽  
Vol 35 (5) ◽  
pp. 1119-1121 ◽  
Author(s):  
G.C. Brown
Keyword(s):  
Nitric Oxide ◽  
Nadph Oxidase ◽  
Neuronal Death ◽  
Glutamate Release ◽  
Inos Expression ◽  
Calcium Dependent ◽  
Vesicular Release ◽  
Oxide Synthase ◽  
Oxide Inhibition ◽  
Inducible Nitric Oxide

Inflammation contributes to a wide variety of brain pathologies, apparently via glia killing neurons. A number of mechanisms by which inflammatory-activated microglia and astrocytes kill neurons have been identified in culture. These include iNOS (inducible nitric oxide synthase), which is expressed in glia only during inflammation, and PHOX (phagocytic NADPH oxidase) found in microglia and acutely activated by inflammation. High levels of iNOS expression in glia cause (i) NO (nitric oxide) inhibition of neuronal respiration, resulting in neuronal depolarization and glutamate release, followed by excitotoxicity, and (ii) glutamate release from astrocytes via calcium-dependent vesicular release. Hypoxia strongly synergizes with iNOS expression to induce neuronal death via mechanism (i), because NO inhibits cytochrome oxidase in competition with oxygen. Activation of PHOX (by cytokines, β-amyloid, prion protein, ATP or arachidonate) causes microglial proliferation and inflammatory activation; thus PHOX is a key regulator of inflammation. Activation of PHOX alone causes no death, but when combined with expressed iNOS results in extensive neuronal death via peroxynitrite production.

scholarly journals ATP stimulates calcium-dependent glutamate release from cultured astrocytes

2001 ◽  
Vol 77 (2) ◽  
pp. 664-675 ◽  
Author(s):  
Aleksandar Jeremic ◽  
Ksenija Jeftinija ◽  
Jelena Stevanovic ◽  
Aleksandra Glavaski ◽  
Srdija Jeftinija
Keyword(s):  
Glutamate Release ◽  
Calcium Dependent ◽  
Cultured Astrocytes

scholarly journals Dissection of a Hypoxia-induced, Nitric Oxide–mediated Signaling Cascade

2009 ◽  
Vol 20 (18) ◽  
pp. 4083-4090 ◽  
Author(s):  
Pascale F. Dijkers ◽  
Patrick H. O'Farrell
Keyword(s):  
Nitric Oxide ◽  
Signal Transduction ◽  
Signaling Cascade ◽  
S2 Cells ◽  
Signal Transduction System ◽  
Signaling Systems ◽  
Calcium Dependent ◽  
Drosophila S2 Cells ◽  
Oxide Synthase ◽  
Multiple Signaling

Befitting oxygen's key role in life's processes, hypoxia engages multiple signaling systems that evoke pervasive adaptations. Using surrogate genetics in a powerful biological model, we dissect a poorly understood hypoxia-sensing and signal transduction system. Hypoxia triggers NO-dependent accumulation of cyclic GMP and translocation of cytoplasmic GFP-Relish (an NFκB/Rel transcription factor) to the nucleus in Drosophila S2 cells. An enzyme capable of eliminating NO interrupted signaling specifically when it was targeted to the mitochondria, arguing for a mitochondrial NO signal. Long pretreatment with an inhibitor of nitric oxide synthase (NOS), L-NAME, blocked signaling. However, addition shortly before hypoxia was without effect, suggesting that signaling is supported by the prior action of NOS and is independent of NOS action during hypoxia. We implicated the glutathione adduct, GSNO, as a signaling mediator by showing that overexpression of the cytoplasmic enzyme catalyzing its destruction, GSNOR, blocks signaling, whereas knockdown of this activity caused reporter translocation in the absence of hypoxia. In downstream steps, cGMP accumulated, and calcium-dependent signaling was subsequently activated via cGMP-dependent channels. These findings reveal the use of unconventional steps in an NO pathway involved in sensing hypoxia and initiating signaling.

Regulation of human placental fetal vessel tone: role of nitric oxide

1995 ◽  
Vol 7 (6) ◽  
pp. 1407 ◽  
Author(s):  
RG King ◽  
NM Gude ◽  
Iulio JL Di ◽  
SP Brennecke
Keyword(s):  
Nitric Oxide ◽  
Perfusion Pressure ◽  
Factors Affecting ◽  
Endothelin 1 ◽  
Calcium Dependent ◽  
Fetal Vessel ◽  
Nitric Oxide Inhibitors ◽  
Vessel Resistance ◽  
Endothelin 3

Factors affecting fetal vessel resistance have been studied in vitro in bilaterally perfused lobules of human placentae. Potent and efficacious constrictors in this preparation (in order of potency) include endothelin-1 > the thromboxane mimetic U46619 > endothelin-3 > prostaglandin F2 alpha. Inhibitors of eicosanoid synthesis did not affect fetal vessel basal perfusion pressure, nor did they potentiate the effects of the vasoconstrictor U46619. In contrast, the nitric oxide inhibitors N omega-nitro-L-arginine (NOLA), haemoglobin and methylene blue all increased fetal vessel basal perfusion pressure and also increased U46619-induced constriction. Similarly, NOLA markedly potentiated the constrictor effects of endothelin-1, angiotensin II, 5-hydroxytryptamine and bradykinin. These studies therefore provide evidence that NO is important in the maintenance of low basal fetal vessel impedance and also reduces the effects of a number of vasoconstrictor autacoids. Nitric oxide synthase (NOS) activity of human placental homogenates has been measured and shown to be mainly calcium-dependent. Human placental NOS activity was not affected by labour state but was reduced in pre-eclampsia. No evidence was found that in pre-eclampsia raised concentrations of the endogenous NOS inhibitor asymmetric dimethylarginine were responsible for the reduced placental NOS activity. Hence, these studies provide evidence that NO is an important endogenous dilator of the fetal vessels of the human placenta and that reduced NOS activity could contribute to the pathogenesis and/or effects of pre-eclampsia.

Nitric oxide modulates synaptic glutamate release during anoxia

1997 ◽  
Vol 228 (1) ◽  
pp. 50-54 ◽  
Author(s):  
Alexander N Katchman ◽  
Norman Hershkowitz
Keyword(s):  
Nitric Oxide ◽  
Glutamate Release

Calcium regulates estrogen increase in permeability of cultured CaSki epithelium by eNOS-dependent mechanism

2000 ◽  
Vol 279 (5) ◽  
pp. C1495-C1505 ◽  
Author(s):  
George I. Gorodeski
Keyword(s):  
Nitric Oxide ◽  
Endothelial Nitric Oxide Synthase ◽  
Cytosolic Calcium ◽  
No Synthase ◽  
Calcium Dependent ◽  
Steady State Levels ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Dependent Mechanism

Estrogen increases baseline transepithelial permeability across CaSki cultures and augments the increase in permeability in response to hypertonic gradients. In estrogen-treated cells, lowering cytosolic calcium abrogated the hypertonicity-induced augmented increase in permeability and decreased baseline permeability to a greater degree than in estrogen-deprived cells. Steady-state levels of cytosolic calcium in estrogen-deprived cells were higher than in estrogen-treated cells. Increases in extracellular calcium increased cytosolic calcium more in estrogen-deprived cells than in estrogen-treated cells. However, in estrogen-treated cells, increasing cytosolic calcium was associated with greater increases in permeability in response to hypertonic gradients than in estrogen-deprived cells. Lowering cytosolic calcium blocked the estrogen-induced increase in nitric oxide (NO) release and in the in vitro conversion of l-[3H]arginine to l-[3H]citrulline. Treatment with estrogen upregulated mRNA of the NO synthase isoform endothelial nitric oxide synthase (eNOS). These results indicate that cytosolic calcium mediates the responses to estrogen and suggest that the estrogen increase in permeability and the augmented increase in permeability in response to hypertonicity involve an increase in NO synthesis by upregulation of the calcium-dependent eNOS.

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