ASIC channel inhibition enhances excitotoxic neuronal death in an in vitro model of spinal cord injury

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• 作者：Graciela L. Mazzone^a ; ^{mazzone@fbmc.fcen.uba.ar} ; Priyadharishini Veeraraghavan^b ; Carlota Gonzalez-Inchauspe^c ; Andrea Nistri^b ; ^d ; ^&dagger ; ; Osvaldo D. Uchitel^c ; ^&dagger ;
• 关键词：ANOVA ; analysis of variance ; ASICs ; acid-sensing ion channels ; AU ; arbitrary unit ; DAPI ; 4&prime ; 6-diamidino-2-phenylindole ; DIV ; days in vitro ; DME/HIGH ; Dulbecco&rsquo ; s modified Eagle&rsquo ; s medium high glucose ; DR ; dorsal root ; FCS ; fetal calf serum ; KA ; kainate ; NGF ; nerve growth factor ; NeuN ; neuronal specific nuclear protein ; PBS ; phosphate-buffered saline ; PI ; propidium iodide ; S100β ; astroglial calcium-binding protein S100β ; SCI ; spinal cord injury ; SEM ; standard error of the mean ; VR
• 刊名：Neuroscience
• 出版年：2017
• 出版时间：20 February 2017
• 年：2017
• 卷：343
• 期：Complete
• 页码：398-410
• 全文大小：2579 K
• 卷排序：343

文摘

ASIC channels are nonselective pores activated by mild acidification and modulating neuronal function. Expression of ASIC channels by mouse spinal cord was increased after a borderline excitotoxic stimulation. ASIC pharmacological blockers or the ASIC1a knockout phenotype intensified excitotoxicity. Electrophysiological network oscillations were suppressed by mild excitotoxic stimuli followed with ASIC block. ASIC activity was an unexpected controller of neurotoxicity to restrain spinal network damage.