Dilek, MustafaKılınç, Yasemin BaranoğluKılınç, ErkanTorun, İbrahim EthemSaylan, AslıhanDüzcü, Selma Erdoğan2024-03-142024-03-142022Dilek, M., Kilinc, Y. B., Kilinc, E., Torun, I. E., Saylan, A., & Duzcu, S. E. (2022). Activation of TRESK background potassium channels by cloxyquin exerts protective effects against excitotoxic-induced brain injury and neuroinflammation in neonatal rats. Journal of Neuroimmunology, 368, 577894.0165-57281872-8421http://dx.doi.org/10.1016/j.jneuroim.2022.577894https://hdl.handle.net/20.500.12491/12088This study was supported by Bolu Abant Izzet Baysal University Scientific Research Fund (Grant-number: 2019.08.23.1433).19th Turkish Neuroscience CongressWe investigated effects of activation of TRESK channels by selective activator cloxyquin on excitotoxic-induced brain injury and neuroinflammation involving brain mast cells and inflammatory cytokines in neonatal rats. Three different doses of cloxyquin (0.2, 1 and 5 mg/kg) were studied in ibotenate-induced perinatal brain injury (PBI) in P5 rat-pups. Cerebral lesions and mast cells in coronal brain sections were evaluated. Concentrations of activin A, IL-1 beta, IL-6 and IL-10 in brain homogenates were measured using ELISA. Cloxyquin dose-dependently exerted protective effects against excitotoxic-induced neonatal brain injury and neuroinflammation. TRESK channels may be a promising new target for the treatment of PBIs.eninfo:eu-repo/semantics/openAccessExcitotoxicityBrain mast cellsNeuroinflammationMast-CellsEarly RespondersActivin-AArticle10.1016/j.jneuroim.2022.577894368110356429942-s2.0-85130530778Q2WOS:000866081500002Q3