| Abstract: | ![]()
Excitotoxic neuronal death mediated by N-methyl-D -aspartate (NMDA) glutamate receptors can contribute to the extended brain damage that often accompanies trauma or disease. Both the inflammatory cytokine tumor necrosis factor-α (TNF-α) and nicotine have been identified as possible neuroprotective agents to NMDA assault. We find that TNF-α protection of a subpopulation of cultured cortical neurons to chronic NMDA-mediated excitotoxic death requires both the activation of the p55/TNFRI, but not p75/TNFRII, and the release of endogenous TNF-α. Nicotine protection to NMDA was mediated through an α-bungarotoxin-sensitive receptor. When coapplied, neuroprotection to NMDA by either TNF-α or nicotine was abolished but could be recovered with α-bungarotoxin. These results suggest that the cytokine TNF-α and α-bungarotoxin-sensitive nicotinic neurotransmitter receptors confer neuroprotection through potentially antagonistic pathways. © 1998 John Wiley & Sons, Inc. J Neurobiol 35: 29–36, 1998 |
