DAF-FM detection of nitric oxide in embryonic cortical neurons

2008 ◽  
Author(s):  
Alexi Nott ◽  
James D. Robinson ◽  
Antonella Riccio
Keyword(s):  
Nitric Oxide ◽  
Cortical Neurons

Effects of deep hypothermia on nitric oxide-induced cytotoxicity in primary cultures of cortical neurons

2003 ◽  
Vol 72 (5) ◽  
pp. 613-621 ◽  
Author(s):  
Sriranganathan Varathan ◽  
Satoshi Shibuta ◽  
Vidya Varathan ◽  
Motohide Takemura ◽  
Norifumi Yonehara ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cortical Neurons ◽  
Primary Cultures ◽  
Deep Hypothermia

scholarly journals Functional significance of nitric oxide in ionomycin-evoked [3H]GABA release from mouse cerebral cortical neurons

2002 ◽  
Vol 81 (1) ◽  
pp. 130-141 ◽  
Author(s):  
Masashi Katsura ◽  
Keijiro Shuto ◽  
Yutaka Mohri ◽  
Makoto Shigeto ◽  
Seitaro Ohkuma
Keyword(s):  
Nitric Oxide ◽  
Cortical Neurons ◽  
Functional Significance ◽  
Gaba Release ◽  
Cerebral Cortical Neurons

Continuous exposure to nitric oxide enhances diazepam binding inhibitor mRNA expression in mouse cerebral cortical neurons

2004 ◽  
Vol 124 (1) ◽  
pp. 29-39 ◽  
Author(s):  
Masashi Katsura ◽  
Keijiro Shuto ◽  
Yutaka Mohri ◽  
Atsushi Tsujimura ◽  
Dai Shibata ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mrna Expression ◽  
Cortical Neurons ◽  
Continuous Exposure ◽  
Cerebral Cortical Neurons

The nitric oxide synthase inhibitor, N-monomethyl-L-arginine blocks induction of a long-term potentiation-like phenomenon in rat medial frontal cortical neurons in vitro

1993 ◽  
Vol 70 (3) ◽  
pp. 1255-1259 ◽  
Author(s):  
A. V. Nowicky ◽  
L. J. Bindman
Keyword(s):  
Nitric Oxide ◽  
Cortical Neurons ◽  
Long Term Potentiation ◽  
Control Group ◽  
Term Potentiation ◽  
The Mean ◽  
Synthase Inhibitor ◽  
Stimulation Of

1. Nitric oxide has been implicated in the production of long-term depression (LTD) in the cerebellum and in the production of long-term potentiation (LTP) and LTD in the hippocampus. We now provide evidence of its involvement in the induction of long-term synaptic potentiation in in vitro slices in the cerebral cortex of the rat. 2. Intracellular recordings were made from layer V neurons in the medial frontal cortex, and excitatory synaptic potentials (EPSPs) were evoked by electrical stimulation of layers II/III. Tetanic stimulation of this pathway may induce LTD or LTP or no change at these synapses. First we established experimental conditions under which a long lasting potentiation could be induced with a high incidence (> 60%), namely perfusion of slices with 1 microM bicuculline methiodide, second the use of increased shock duration in the tetanic conditioning stimuli, third and most important the addition of QX-314 to the microelectrode to reduce potassium conductances. Because the potentiation of the mean EPSP slope was significantly greater than the control at 40-min postconditioning, but was declining throughout this period, we refer to it for brevity as LTP, but strictly class it as an LTP-like phenomenon. 3. The nitric oxide (NO) synthase inhibitor interfered with the production of LTP. In the control group of neurons (n = 13) the mean depolarizing slope of the EPSP at 30-min post-conditioning was 142.7 +/- 2% (mean +/- SE) of the prestimulation control.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Depolarization of mitochondria in neurons promotes activation of nitric oxide synthase and generation of nitric oxide

2016 ◽  
Vol 310 (9) ◽  
pp. H1097-H1106 ◽  
Author(s):  
Prasad V. G. Katakam ◽  
Somhrita Dutta ◽  
Venkata N. Sure ◽  
Samuel M. Grovenburg ◽  
Angellica O. Gordon ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cortical Neurons ◽  
Ex Vivo ◽  
Cerebral Arteries ◽  
Resonance Spectroscopy ◽  
No Production ◽  
Cultured Neurons ◽  
Mitochondrial Depolarization ◽  
Oxide Synthase

The diverse signaling events following mitochondrial depolarization in neurons are not clear. We examined for the first time the effects of mitochondrial depolarization on mitochondrial function, intracellular calcium, neuronal nitric oxide synthase (nNOS) activation, and nitric oxide (NO) production in cultured neurons and perivascular nerves. Cultured rat primary cortical neurons were studied on 7–10 days in vitro, and endothelium-denuded cerebral arteries of adult Sprague-Dawley rats were studied ex vivo. Diazoxide and BMS-191095 (BMS), activators of mitochondrial KATP channels, depolarized mitochondria in cultured neurons and increased cytosolic calcium levels. However, the mitochondrial oxygen consumption rate was unaffected by mitochondrial depolarization. In addition, diazoxide and BMS not only increased the nNOS phosphorylation at positive regulatory serine 1417 but also decreased nNOS phosphorylation at negative regulatory serine 847. Furthermore, diazoxide and BMS increased NO production in cultured neurons measured with both fluorescence microscopy and electron spin resonance spectroscopy, which was sensitive to inhibition by the selective nNOS inhibitor 7-nitroindazole (7-NI). Diazoxide also protected cultured neurons against oxygen-glucose deprivation, which was blocked by NOS inhibition and rescued by NO donors. Finally, BMS induced vasodilation of endothelium denuded, freshly isolated cerebral arteries that was diminished by 7-NI and tetrodotoxin. Thus pharmacological depolarization of mitochondria promotes activation of nNOS leading to generation of NO in cultured neurons and endothelium-denuded arteries. Mitochondrial-induced NO production leads to increased cellular resistance to lethal stress by cultured neurons and to vasodilation of denuded cerebral arteries.

Mitochondrial involvement in nitric oxide-induced cellular death in cortical neurons in culture

2006 ◽  
Vol 83 (3) ◽  
pp. 441-449 ◽  
Author(s):  
S. Figueroa ◽  
M.J. Oset-Gasque ◽  
C. Arce ◽  
C.J. Martinez-Honduvilla ◽  
M.P. González
Keyword(s):  
Nitric Oxide ◽  
Cortical Neurons ◽  
Cellular Death

scholarly journals Role of nitric oxide-mediated glutathionylation in neuronal function: potential regulation of energy utilization

2010 ◽  
Vol 428 (1) ◽  
pp. 85-93 ◽  
Author(s):  
Li-Peng Yap ◽  
Jerome V. Garcia ◽  
Derick S. Han ◽  
Enrique Cadenas
Keyword(s):  
Nitric Oxide ◽  
Redox Potential ◽  
Cortical Neurons ◽  
Biological Significance ◽  
Energy Utilization ◽  
Small Subset ◽  
Cellular Redox ◽  
Age Related ◽  
Nitric Oxide Radical ◽  
The Impact

Excessive generation of nitric oxide radical (NO•) in neuroinflammation, excitotoxicity and during age-related neurodegenerative disorders entails the localized and concerted increase in nitric oxide synthase(s) expression in glial cells and neurons. The aim of the present study was to assess the biological significance of the impact of NO• on the cell's thiol status with emphasis on S-glutathionylation of targeted proteins. Exposure of primary cortical neurons or astrocytes to increasing flow rates of NO• (0.061–0.25 μM/s) resulted in the following. (i) A decrease in GSH (glutathione) in neurons accompanied by formation of GSNO (S-nitrosoglutathione) and GSSG (glutathione disulfide); neurons were far more sensitive to NO• exposure than astrocytes. (ii) A dose-dependent oxidation of the cellular redox status: the neuron's redox potential increased ~42 mV and that of astrocytes ~23 mV. A good correlation was observed between cell viability and the cellular redox potential. The higher susceptibility of neurons to NO• can be partly explained by a reduced capacity to recover GSH through lower activities of GSNO and GSSG reductases. (iii) S-glutathionylation of a small subset of proteins, among them GAPDH (glyceraldehyde-3-phosphate dehydrogenase), the S-glutathionylation of which resulted in inhibition of enzyme activity. The quantitative analyses of changes in the cell's thiol potential upon NO• exposure and their consequences for S-glutathionylation are discussed in terms of the distinct redox environment of astrocytes and neurons.

Reactive oxygen species are involved in nitric oxide-induced apoptosis in rat cortical neurons

2000 ◽  
Vol 26 (9) ◽  
pp. 875-883
Author(s):  
Taotao Wei ◽  
Chunyang Zhang ◽  
Jingwu Hou ◽  
Chang Chen ◽  
Hui Ma ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Cortical Neurons ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Rat Cortical Neurons ◽  
Induced Apoptosis

Chronic Ethanol IncreasesN-Methyl-d-Aspartate-Stimulated Nitric Oxide Formation but Not Receptor Density in Cultured Cortical Neurons

1997 ◽  
Vol 51 (5) ◽  
pp. 733-740 ◽  
Author(s):  
L. Judson Chandler ◽  
Greg Sutton ◽  
Dean Norwood ◽  
Colin Sumners ◽  
Fulton T. Crews
Keyword(s):  
Nitric Oxide ◽  
Cortical Neurons ◽  
Chronic Ethanol ◽  
Receptor Density ◽  
Oxide Formation ◽  
Nitric Oxide Formation ◽  
Cultured Cortical Neurons
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