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Previous studies have demonstrated that increased chloride channel activity plays a role in nitric oxide-induced neuronal apoptosis in the rat hippocampus. The present study investigated the effects of the broad-spectrum calcium channel blocker CdCl2 on survival rate, percentage of apoptosis, and morphological changes in hippocampal neurons cultured in vitro, as well as the effects of calcium channels on neuronal apoptosis. The chloride channel blockers 4-acetamido-4’-isothiocyanatostilbene-2, 2’-disulfonic acid (SITS) or 4, 4’-diisothiocyanostilbene-2, 2’-disulfonic acid (DIDS) increased the survival rate of 3-morpholinosydnonimine (SIN-1)-treated neurons and suppressed SIN-1-induced neuronal apoptosis. The calcium channel blocker CdCl2 did not increase the survival rate of neurons and did not affect SIN-1-induced apoptosis or SITS- or DIDS-suppressed neuronal apoptosis. Results demonstrated that calcium channels did not significantly affect neuronal apoptosis.
Previous studies have demonstrated that increased chloride channel activity plays a role in nitric oxide-induced neuronal apoptosis in the rat hippocampus. The present study investigated the effects of the broad-spectrum calcium channel blocker CdCl2 on survival rate, percentage of apoptosis, and morphological changes in hippocampal neurons cultured in vitro as well as the effects of calcium channels on neuronal apoptosis. The chloride channel blockers 4-acetamido-4’-isothiocyanatostilbene-2, 2’-disulfonic acid (SITS) or 4, 4’-diisothiocyanostilbene- 2, 2’-disulfonic acid (DIDS) increased the survival rate of 3-morpholinosydnonimine (SIN-1) -treated neurons and suppressed SIN- 1 -induced neuronal apoptosis. The calcium channel blocker CdCl2 did not increase the survival rate of neurons and did not affect SIN-1-induced apoptosis or SITS- or DIDS-suppressed neuronal apoptosis.