| Autor: |
Suraj S. Vasanthi, Nikhil S. Rao, Manikandan Samidurai, Nyzil Massey, Christina Meyer, Meghan Gage, Mihir Kharate, Aida Almanza, Logan Wachter, Candide Mafuta, Lily Trevino, Adriana M. Carlo, Elijah Bryant, Brooke E. Corson, Morgan Wohlgemuth, Morgan Ostrander, Lucas Showman, Chong Wang, Thimmasettappa Thippeswamy |
| Jazyk: |
angličtina |
| Rok vydání: |
2023 |
| Předmět: |
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| Zdroj: |
Journal of Neuroinflammation, Vol 20, Iss 1, Pp 1-25 (2023) |
| Druh dokumentu: |
article |
| ISSN: |
1742-2094 |
| DOI: |
10.1186/s12974-023-02847-1 |
| Popis: |
Abstract Background Acute exposure to seizurogenic organophosphate (OP) nerve agents (OPNA) such as diisopropylfluorophosphate (DFP) or soman (GD), at high concentrations, induce immediate status epilepticus (SE), reactive gliosis, neurodegeneration, and epileptogenesis as a consequence. Medical countermeasures (MCMs—atropine, oximes, benzodiazepines), if administered in 20 min of continuous convulsive seizures. 1400W significantly reduced GD-induced motor and cognitive dysfunction; nitrooxidative stress (nitrite, ROS; increased GSH: GSSG); proinflammatory cytokines in the serum and some in the cerebrospinal fluid (CSF); epileptiform spikes and spontaneously recurring seizures (SRS) in males; reactive gliosis (GFAP + C3 and IBA1 + CD68-positive glia) as a measure of neuroinflammation, and neurodegeneration (especially parvalbumin-positive neurons) in some brain regions. Conclusion These findings demonstrate the long-term disease-modifying effects of a glial-targeted iNOS inhibitor, 1400W, in a rat GD model by modulating reactive gliosis, neurodegeneration (parvalbumin-positive neurons), and neuronal hyperexcitability. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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