The permeable calcium chelator BAPTA/AM is known to prevent free radical-mediated toxicity promote apoptosis in non-neuronal cells and produce a beneficial effect in neuronal cells by protecting neurons from ischemic damage. In addition, it has been suggested that BAPTA/AM induces a late, but not early, increase of intracellular calcium in I-IL-60 neoplastic cells. Mixed cortical cell cultures (DIV 13-16) exposed to 10μM BAPTA/AM for 24- or 48-hr show moderate (45-70%) neuronal injury as evaluated by increased LDH release into the bathing medium after 24-48-hr. Exposure of cortical cultures to 3-10 μM BAPTA/AM for 48-hr evoke dose-dependent neuronal damage[1].
Kinase Assay
Cell Assay
Neuronal injury is quantitatively estimated by measuring lactate dehydrogenase (LDH) released from damaged cells into the bathing medium 24- or 48-hr after the 10 μM BAPTA/AM treatment. The morphological findings are confirmed by staining with neuron-specific enolase (NSE) antibody and tryphan blue[1].
Animal Administration
References
[1]. Wie MB, et al. BAPTA/AM, an intracellular calcium chelator, induces delayed necrosis by lipoxygenase-mediated free radicals in mouse cortical cultures. Prog Neuropsychopharmacol Biol Psychiatry. 2001 Nov;25(8):1641-59.
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