Increased activities of ClC-3 chloride channel may be involved in hippocampal neuronal apoptosis

Over-production of nitric oxide and ion disturbance are involved in neuronal apoptosis around the ischemic area following ischemic brain injury. Prof. Quanzhong Chang and team from Zhuhai Campus of Zunyi Medical College in China established a rat model of hippocampal neuronal apoptosis by using 3-morpholinosyndnomine (SIN-1), a nitric oxide donor.

The models were then administered the chloride channel blocker, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), in a broader attempt to observe ClC-3 chloride channel expression in the neuronal apoptosis process and to investigate the correlation between chloride channel activity and ischemia-sensitive neuronal apoptosis. Their results showed that SIN-1 reduced the neuronal survival rate, induced neuronal apoptosis, and promoted ClC-3 chloride channel protein and mRNA expression in the apoptotic neurons. DIDS reversed the effect of SIN-1. These findings, published in the Neural Regeneration Research (Vol. 8, No. 32, 2013), indicate that the increased activities of the ClC-3 chloride channel may be involved in hippocampal neuronal apoptosis induced by nitric oxide.



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