scholarly journals Modulation of Presynaptic GABA Release by Oxidative Stress in Mechanically-isolated Rat Cerebral Cortical Neurons

2010 ◽  
Vol 14 (3) ◽  
pp. 127 ◽  
Author(s):  
Eu-Teum Hahm ◽  
Jung-Woo Seo ◽  
Jinyoung Hur ◽  
Young-Wuk Cho
Keyword(s):  
Oxidative Stress ◽  
Cortical Neurons ◽  
Gaba Release ◽  
Cerebral Cortical Neurons ◽  
Isolated Rat

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

Removal of hydroxyl radical increases nitric oxide generators-induced [3H]GABA release from mouse cerebral cortical neurons

1995 ◽  
Vol 194 (1-2) ◽  
pp. 101-104 ◽  
Author(s):  
Seitaro Ohkuma ◽  
Masashi Katsura ◽  
Da-Zhi Chen ◽  
Hidehiko Narihara ◽  
Kinya Kuriyama
Keyword(s):  
Nitric Oxide ◽  
Hydroxyl Radical ◽  
Cortical Neurons ◽  
Gaba Release ◽  
Cerebral Cortical Neurons

Nitric Oxide-Induced [3H]GABA Release from Cerebral Cortical Neurons Is Mediated by Peroxynitrite

2002 ◽  
Vol 65 (3) ◽  
pp. 1109-1114 ◽  
Author(s):  
Seitaro Ohkuma ◽  
Hidehiko Narihara ◽  
Masashi Katsura ◽  
Takeshi Hasegawa ◽  
Kinya Kuriyama
Keyword(s):  
Nitric Oxide ◽  
Cortical Neurons ◽  
Gaba Release ◽  
Cerebral Cortical Neurons

Nrf2 mediates the neuroprotective effect of isoflurane preconditioning in cortical neuron injury induced by oxygen-glucose deprivation

2021 ◽  
pp. 096032712198941
Author(s):  
X-S Liu ◽  
X-L Bai ◽  
Z-X Wang ◽  
S-Y Xu ◽  
Y Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cortical Neuron ◽  
Cortical Neurons ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Lactate Dehydrogenase Activity ◽  
Primary Mouse ◽  
Ldh Release ◽  
Neuron Injury ◽  
And Oxidative Stress

Objective: To investigate how nuclear factor-E2-related factor 2 (Nrf2) involved in the protective effect of isoflurane (Iso) preconditioning in oxygen glucose deprivation (OGD)-induced cortical neuron injury. Methods: Primary mouse cortical neurons were divided into Control, ML385 (an Nrf2 inhibitor), Iso, Iso + ML385, OGD, ML385 + OGD, Iso + OGD, and Iso + ML385 + OGD groups. Lactate dehydrogenase activity (LDH) release and oxidative stress indexes were quantified. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to detect cell viability, Annexin V-FITC/propidium iodide (PI) staining to measure cell apoptosis, dichloro-dihydro-fluorescein diacetate (DCFH-DA) method to test reactive oxygen species (ROS), and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and Western blotting to evaluate genes and protein expression. Results: Iso preconditioning reduced LDH release and inhibited cell cytotoxicity in OGD-induced cortical neurons, which was abolished by ML385. Iso preconditioning increased the Nrf2 nuclear translocation in cortical neurons. Meanwhile, Iso decreased the OGD-induced apoptosis with the down-regulations of Bax and Caspase-3 and the up-regulation of Bcl-2, which was reversed by ML385. OGD enhanced the level of ROS and malondialdehyde (MDA) in cortical neurons, but reduced the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), which were aggravated in ML385 + OGD group and mitigated in Iso + OGD group. No observable difference was found between OGD group and Iso + ML385 + OGD group regarding apoptosis-related proteins and oxidative stress-related indexes. Conclusion: Iso preconditioning up-regulated Nrf2 level to play its protective role in OGD-induced mouse cortical neuron injury.

scholarly journals Neurotherapeutic Effect of Inula britannica var. Chinensis against H2O2-Induced Oxidative Stress and Mitochondrial Dysfunction in Cortical Neurons

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 375
Author(s):  
Jin Young Hong ◽  
Hyunseong Kim ◽  
Junseon Lee ◽  
Wan-Jin Jeon ◽  
Seung Ho Baek ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Cortical Neurons ◽  
Inflammatory Diseases ◽  
Neuroprotective Effect ◽  
Neuroprotective Effects ◽  
Neuronal Viability ◽  
Inula Britannica ◽  
Oxidative Effects

Inula britannica var. chinensis (IBC) has been used as a traditional medicinal herb to treat inflammatory diseases. Although its anti-inflammatory and anti-oxidative effects have been reported, whether IBC exerts neuroprotective effects and the related mechanisms in cortical neurons remain unknown. In this study, we investigated the effects of different concentrations of IBC extract (5, 10, and 20 µg/mL) on cortical neurons using a hydrogen peroxide (H2O2)-induced injury model. Our results demonstrate that IBC can effectively enhance neuronal viability under in vitro-modeled reaction oxygen species (ROS)-generating conditions by inhibiting mitochondrial ROS production and increasing adenosine triphosphate level in H2O2-treated neurons. Additionally, we confirmed that neuronal death was attenuated by improving the mitochondrial membrane potential status and regulating the expression of cytochrome c, a protein related to cell death. Furthermore, IBC increased the expression of brain-derived neurotrophic factor and nerve growth factor. Furthermore, IBC inhibited the loss and induced the production of synaptophysin, a major synaptic vesicle protein. This study is the first to demonstrate that IBC exerts its neuroprotective effect by reducing mitochondria-associated oxidative stress and improving mitochondrial dysfunction.

Developmental Expression of Calcium-Binding Protein-Containing Neurons in Neocortical Transplants

1998 ◽  
Vol 7 (2) ◽  
pp. 121-129 ◽  
Author(s):  
Jeffrey M. Rosenstein ◽  
Newton S. More ◽  
Nina Mani ◽  
Janette M. Krum
Keyword(s):  
Oxidative Stress ◽  
Cortical Neurons ◽  
Calcium Binding ◽  
Binding Protein ◽  
Substantial Reduction ◽  
Qualitative Change ◽  
Afferent Input ◽  
Calcium Binding Protein ◽  
Developmental Expression ◽  
Parvalbumin Neurons

The present study examined the development of calcium binding protein-containing neurons in a timed series of fetal neocortical transplants. The immunoexpression of parvalbumin and calbindin, which are subpopulations of GABAergic neurons, have been widely studied in normal development and in disease and injury states. Because of their purported resistance to oxidative injury by their ability to buffer Ca++ influx, these neurons have been particularly studied following ischemia. Because it is likely that oxidative stress is associated with the grafting procedure, we sought to determine if these neurons displayed enhanced survival characteristics. Normally, parvalbumin and calbindin represent about 5-10% of cortical neurons. Within 2-4 wk after grafting the expression of both proteins increased markedly in that a relatively larger number of neurons (27% for parvalbumin) were immunopositive. This increase was transitory, however, and by 4 mo and beyond, confocal microscopic data showed a reduction of over 50% of parvalbumin (+) neurons and processes. Calbindin (+) processes showed a qualitative change in that they were smaller with less terminal branching. Electron microscopy confirmed a substantial reduction in parvalbumin synaptic contacts. Interestingly, in older grafts, remaining parvalbumin neurons were those that were strongly NSE (+) suggesting a link between normal metabolism and Ca++ buffering in grafted neurons. It is possible that in early grafts certain neuronal populations transiently upregulated calcium binding proteins as a defensive mechanism against Ca++ influx associated with oxidative stress. Over time, however, following physiological normalization within grafts, the calcium binding protein (+) neurons are diminished, possibly due to lack of appropriate afferent input to the interneuronal pool.

scholarly journals Chronic exposure to U18666A is associated with oxidative stress in cultured murine cortical neurons

2006 ◽  
Vol 98 (4) ◽  
pp. 1278-1289 ◽  
Author(s):  
Chor Hui Vivien Koh ◽  
Matthew Whiteman ◽  
Qiao-Xin Li ◽  
Barry Halliwell ◽  
Andrew M. Jenner ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cortical Neurons ◽  
Chronic Exposure

Low level laser therapy reduces oxidative stress in cortical neurons in vitro

2012 ◽  
Author(s):  
Ying-Ying Huang ◽  
Clark E. Tedford ◽  
Thomas McCarthy ◽  
Michael R. Hamblin
Keyword(s):  
Oxidative Stress ◽  
Laser Therapy ◽  
Cortical Neurons ◽  
Low Level Laser Therapy ◽  
Low Level ◽  
Low Level Laser ◽  
Level Laser

Neuroprotective effects of vitexin by inhibition of NMDA receptors in primary cultures of mouse cerebral cortical neurons

2013 ◽  
Vol 386 (1-2) ◽  
pp. 251-258 ◽  
Author(s):  
Le Yang ◽  
Zhi-ming Yang ◽  
Nan Zhang ◽  
Zhen Tian ◽  
Shui-bing Liu ◽  
...  
Keyword(s):  
Nmda Receptors ◽  
Cortical Neurons ◽  
Primary Cultures ◽  
Neuroprotective Effects ◽  
Cerebral Cortical Neurons
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