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  • Title: Activation of voltage-sensitive sodium channels during oxygen deprivation leads to apoptotic neuronal death.
    Author: Banasiak KJ, Burenkova O, Haddad GG.
    Journal: Neuroscience; 2004; 126(1):31-44. PubMed ID: 15145071.
    Abstract:
    Sodium (Na(+)) entry into neurons during hypoxia is known to be associated with cell death. However, it is not clear whether Na(+) entry causes cell death and by what mechanisms this increased Na(+) entry induces death. In this study we used cultures of rat neocortical neurons to show that an increase in intracellular sodium (Na(i)(+)) through voltage-sensitive sodium channels (VSSCs), during hypoxia contributes to apoptosis. Hypoxia increased Na(i)(+) and induced neuronal apoptosis, as assessed by electron microscopy, annexin V staining, and terminal UDP nick end labeling staining. Reducing Na(+) entry with the VSSC blocker, tetrodotoxin (TTX), attenuated apoptotic neuronal death via a reduction in caspase-3 activation. Since the attenuation of apoptosis by TTX during hypoxia suggested that the activation of VSSCs and Na(+) entry are crucial events in hypoxia-induced cell death, we also determined whether the activation of VSSCs per se could lead to apoptosis under resting conditions. Increasing Na(+) entry with the VSSC activator veratridine also induced neuronal apoptosis and caspase-3 activation. These data indicate that a) Na(+) entry via VSSCs during hypoxia leads to apoptotic cell death which is mediated, in part, by caspase-3 and b) activation of VSSCs during oxygen deprivation is a major event by which hypoxia induces cell death.
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