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Research Implicates ClC-3 Chloride Channel in Hippocampal Neuronal Cell Death

by Kathy Jones on  January 4, 2014 at 4:02 PM Research News   - G J E 4
Previous research has explained how over-production of nitric oxide and ion disturbance result in neuronal cell death around the ischemic area following ischemic brain injury.
 Research Implicates ClC-3 Chloride Channel in Hippocampal Neuronal Cell Death
Research Implicates ClC-3 Chloride Channel in Hippocampal Neuronal Cell Death
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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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Source: Eurekalert
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