Background: Important species differences make a human model of in vitro hypoxic neuronal cell death desirable.
Materials and Methods: Human NT2 teratocarcinoma cells were differentiated to NT2-N neurons and exposed to hypoxia for 6 hours. Cell death was evaluated after 48 hours by microscopy and by LDH release (% of total LDH).
Results: Marked cell death was seen in hypoxic cultures. LDH release after hypoxia was 24.2±5.5% vs 13.8±3.7% in nonhypoxic controls (p<0.01). If glutamine was omitted from the medium (preventing glutamate release) or the NMDA receptor blocker MK-801 was added before hypoxia, cell death was almost completely prevented (LDH release 15.4±4.5% and 15.5±5.2%, p<0.001). The non-NMDA receptor blocker CNQX also provided marked protection (18.7±5.1%, p<0.001) while the 21-aminosteroid U74389G, N-acetylcystein, the spin trap PBN or the nitric oxide synthase inhibitor L-nitroarginine were ineffective.
Conclusion: Both NMDA and non-NMDA receptors are important for hypoxic cell death in human NT2-N neurons.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Rootwelt, T., Dunn, M., Yudkoff, M. et al. Hypoxic cell death in the human NT2-N neuronal cell line. Pediatr Res 42, 387 (1997). https://doi.org/10.1203/00006450-199709000-00031
Issue Date:
DOI: https://doi.org/10.1203/00006450-199709000-00031