Heat stress reduces glutamate toxicity in cultured neurons without hsp70 expression.
Consistent with known cytoprotective effects, mild heat stress reduced the vulnerability of cultured cortical neurons to glutamate-induced cell death. However, this neuroprotective effect occurred without expression of the inducible heat stress protein, hsp70, as detected by immunocytochemistry, immunoblotting, or metabolic labeling. Present data suggest that the anti-excitotoxic effect of mild heat stress is mediated outside of the traditional hsp70 mechanism.
Snider
B J
BJ
Center for the Study of Nervous System Injury, Washington University School of Medicine, St. Louis, MO 63110, USA.
Choi
D W
DW
D000818:Animals; D001253:Astrocytes / Q000187:drug effects*; D016923:Cell Death / Q000187:drug effects*; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D018698:Glutamic Acid / Q000633:toxicity*; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism*; D018882:Heat Stress Disorders; D007150:Immunohistochemistry; D051379:Mice; D008815:Mice, Inbred Strains
D018840:HSP70 Heat-Shock Proteins; D018698:Glutamic Acid