scholarly journals Fluorescent Analysis Reveals that Insulin Diminishes Superoxide Increase in Neurons Induced with Toxic Glutamate Treatment

2021 ◽  
Author(s):  
Vsevolod G. Pinelis ◽  
Irina Krasil'nikova ◽  
Zanda Bakaeva ◽  
Alexander M. Surin ◽  
Andrey P. Fisenko ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Glutamate Release ◽  
Superoxide Production ◽  
Glutamate Excitotoxicity ◽  
Comorbid Condition ◽  
Fluorescent Indicators ◽  
Calcium Deregulation ◽  
Mitochondrial Superoxide ◽  
Strong Linear Correlation ◽  
Cultured Cortical Neurons

Glutamate excitotoxicity is implicated in the pathogenesis of many disorders, including stroke, traumatic brain injury, and Alzheimer’s disease, for which central insulin resistance is a comorbid condition. Massive glutamate release primarily through ionotropic N-methyl-D-aspartate receptors (NMDARs) causes a sustained rise in [Ca2+]i, followed by mitochondrial depolarization and an increase in intracellular O2• (superoxide) production. Recently, we found that insulin protected neurons against excitotoxicity by diminishing the delayed calcium deregulation (DCD), However, a role of insulin in superoxide production in excitotoxicity still needs to be clarified. The present study is aimed to investigate the effects of insulin on glutamate-evoked superoxide generation and DCD using the fluorescent indicators dihydroethidium, MitoSOX Red, and Fura-FF in rats cultured cortical neurons. We found that insulin significantly diminished both the intracellular and mitochondrial superoxide production in neurons exposed to glutamate and there was a strong linear correlation between [Ca2+]i and intracellular superoxide. MK 801, an inhibitor of NMDAR-gated Ca2+ influx, completely abrogated the glutamate effects in both the presence and absence of insulin. In experiments on sister cultures, insulin diminishes neuronal death. Thus, collectively, data obtained suggest that insulin diminishes glutamate-induced superoxide production in neurons via fall of [Ca2+]i increased and thereby improves viability of neurons

Neuroprotective Potential of Peptides HFRWPGP (ACTH6–9PGP), KKRRPGP, and PyrRP in Cultured Cortical Neurons at Glutamate Excitotoxicity

2020 ◽  
Vol 491 (1) ◽  
pp. 62-66
Author(s):  
Z. V. Bakaeva ◽  
A. M. Surin ◽  
N. V. Lizunova ◽  
A. E. Zgodova ◽  
I. A. Krasilnikova ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Glutamate Excitotoxicity ◽  
Cultured Cortical Neurons

scholarly journals Green Tea Polyphenols Attenuated Glutamate Excitotoxicity via Antioxidative and Antiapoptotic Pathway in the Primary Cultured Cortical Neurons

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Lin Cong ◽  
Chang Cao ◽  
Yong Cheng ◽  
Xiao-Yan Qin
Keyword(s):  
Green Tea ◽  
Cortical Neurons ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Tea Polyphenols ◽  
Green Tea Polyphenols ◽  
Glutamate Excitotoxicity ◽  
Sod Activity ◽  
Antiapoptotic Proteins ◽  
Cultured Cortical Neurons

Green tea polyphenols are a natural product which has antioxidative and antiapoptotic effects. It has been shown that glutamate excitotoxicity induced oxidative stress is linked to neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. In this study we explored the neuroprotective effect of green teen polyphenols against glutamate excitotoxicity in the primary cultured cortical neurons. We found that green tea polyphenols protected against glutamate induced neurotoxicity in the cortical neurons as measured by MTT and TUNEL assays. Green tea polyphenols were then showed to inhibit the glutamate induced ROS release and SOD activity reduction in the neurons. Furthermore, our results demonstrated that green tea polyphenols restored the dysfunction of mitochondrial pro- or antiapoptotic proteins Bax, Bcl-2, and caspase-3 caused by glutamate. Interestingly, the neuroprotective effect of green tea polyphenols was abrogated when the neurons were incubated with siBcl-2. Taken together, these results demonstrated that green tea polyphenols protected against glutamate excitotoxicity through antioxidative and antiapoptotic pathways.

scholarly journals Rosuvastatin induces delayed preconditioning against l-glutamate excitotoxicity in cultured cortical neurons

2010 ◽  
Vol 56 (3) ◽  
pp. 404-409 ◽  
Author(s):  
Ferenc Domoki ◽  
Béla Kis ◽  
Tamás Gáspár ◽  
James A. Snipes ◽  
Ferenc Bari ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Glutamate Excitotoxicity ◽  
Cultured Cortical Neurons

scholarly journals Basic Fibroblast Growth Factor Evokes a Rapid Glutamate Release through Activation of the MAPK Pathway in Cultured Cortical Neurons*

2002 ◽  
Vol 277 (32) ◽  
pp. 28861-28869 ◽  
Author(s):  
Tadahiro Numakawa ◽  
Daisaku Yokomaku ◽  
Kazuyuki Kiyosue ◽  
Naoki Adachi ◽  
Tomoya Matsumoto ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Cortical Neurons ◽  
Mapk Pathway ◽  
Glutamate Release ◽  
Fibroblast Growth ◽  
Cultured Cortical Neurons

Phencyclidine rapidly induced glutamate release and increased BDNF expression in cultured cortical neurons

2007 ◽  
Vol 58 ◽  
pp. S122
Author(s):  
Naoki Adachi ◽  
Tadahiro Numakawa ◽  
Emi Kumamaru ◽  
Aiko Izumi ◽  
Hiroshi Kunugi
Keyword(s):  
Cortical Neurons ◽  
Glutamate Release ◽  
Bdnf Expression ◽  
Cultured Cortical Neurons

scholarly journals Brain-derived neurotrophic factor enhances depolarization-evoked glutamate release in cultured cortical neurons

2008 ◽  
Vol 79 (3) ◽  
pp. 522-530 ◽  
Author(s):  
Tomoya Matsumoto ◽  
Tadahiro Numakawa ◽  
Naoki Adachi ◽  
Daisaku Yokomaku ◽  
Satoru Yamagishi ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Cortical Neurons ◽  
Glutamate Release ◽  
Brain Derived Neurotrophic Factor ◽  
Cultured Cortical Neurons

scholarly journals The Bacterial Enzyme Cas13 Interferes with Neurite Outgrowth from Cultured Cortical Neurons

Toxins ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 262
Author(s):  
Qin-Wei Wu ◽  
Josef P. Kapfhammer
Keyword(s):  
Rna Editing ◽  
Cortical Neurons ◽  
High Efficiency ◽  
Primary Cultures ◽  
Cultured Neurons ◽  
Therapeutic Tool ◽  
Bacterial Enzyme ◽  
Rna Targeting ◽  
Cultured Cortical Neurons ◽  
New Generation

The CRISPR-Cas13 system based on a bacterial enzyme has been explored as a powerful new method for RNA manipulation. Due to the high efficiency and specificity of RNA editing/interference achieved by this system, it is currently being developed as a new therapeutic tool for the treatment of neurological and other diseases. However, the safety of this new generation of RNA therapies is still unclear. In this study, we constructed a vector expressing CRISPR-Cas13 under a constitutive neuron-specific promoter. CRISPR-Cas13 from Leptotrichia wadei was expressed in primary cultures of mouse cortical neurons. We found that the presence of CRISPR-Cas13 impedes the development of cultured neurons. These results show a neurotoxic action of Cas13 and call for more studies to test for and possibly mitigate the toxic effects of Cas13 enzymes in order to improve CRISPR-Cas13-based tools for RNA targeting.

scholarly journals Genomic instability induced by radiation-mimicking chemicals is not associated with persistent mitochondrial degeneration

2021 ◽  
Author(s):  
Luukkonen Jukka ◽  
Höytö Anne ◽  
Sokka Miiko ◽  
Syväoja Juhani ◽  
Juutilainen Jukka ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Ionizing Radiation ◽  
Genomic Instability ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Neuroblastoma Cells ◽  
Superoxide Production ◽  
Mitochondrial Activity ◽  
Mitochondrial Superoxide

AbstractIonizing radiation has been shown to cause induced genomic instability (IGI), which is defined as a persistently increased rate of genomic damage in the progeny of the exposed cells. In this study, IGI was investigated by exposing human SH-SY5Y neuroblastoma cells to hydroxyurea and zeocin, two chemicals mimicking different DNA-damaging effects of ionizing radiation. The aim was to explore whether IGI was associated with persistent mitochondrial dysfunction. Changes to mitochondrial function were assessed by analyzing mitochondrial superoxide production, mitochondrial membrane potential, and mitochondrial activity. The formation of micronuclei was used to determine immediate genetic damage and IGI. Measurements were performed either immediately, 8 days, or 15 days following exposure. Both hydroxyurea and zeocin increased mitochondrial superoxide production and affected mitochondrial activity immediately after exposure, and mitochondrial membrane potential was affected by zeocin, but no persistent changes in mitochondrial function were observed. IGI became manifested 15 days after exposure in hydroxyurea-exposed cells. In conclusion, immediate responses in mitochondrial function did not cause persistent dysfunction of mitochondria, and this dysfunction was not required for IGI in human neuroblastoma cells.

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