1999
DOI: 10.1016/s0006-8993(99)02126-5
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Tumor necrosis factor-α attenuates N-methyl-d-aspartate-mediated neurotoxicity in neonatal rat hippocampus

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Cited by 27 publications
(19 citation statements)
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“…Co-injections of TNF-! and NMDA into the hippocampus reduced excitotoxic injury; however, intrastriatal co-injections did not alter the severity of injury (Liu et al 1999). TNF-!…”
Section: Neuroprotective Effects Of Tnf-amentioning
confidence: 89%
“…Co-injections of TNF-! and NMDA into the hippocampus reduced excitotoxic injury; however, intrastriatal co-injections did not alter the severity of injury (Liu et al 1999). TNF-!…”
Section: Neuroprotective Effects Of Tnf-amentioning
confidence: 89%
“…Interestingly, inhibition of TNF-a by antibodies prevents ischemic injury (Barone et al, 1997), while mice deficient in TNFR1 are resistant to sepsis-induced encephalopathy (Alexander et al, 2008) and excitotoxic damage is prevented in brain slices from TNFR1 knockout mice (Bernardino et al, 2005). However, TNF-a was shown to attenuate NMDA-mediated neurotoxicity (Liu et al, 1999b) and TNFR1 knock-out mice are reported to be more vulnerable to brain ischemia (Bruce et al, 1996). Differential effects were also observed since inhibition of TNF-a was found to simultaneous attenuate or exacerbate injury depending on the brain region (Galasso et al, 2000).…”
Section: Discussionmentioning
confidence: 99%
“…When cells are exposed to excess glutamate, a cell will die from either rapid necrosis via an influx of Na + and Cl -or delayed apoptosis via a Ca 2+ -dependent pathway. Glutamate excitotoxicity can arise due to a variety of circumstances, including blunt force trauma, lack of proper cell oxygenation, hypoglycemia, and inappropriate release of glutamate from degenerating neurons [8][9][10].…”
mentioning
confidence: 99%