作者: M.V Hejmadi , F Dajas-Bailador , S.M Barns , B Jones , S Wonnacott
DOI: 10.1016/S1044-7431(03)00244-6
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摘要: Abstract Activation of neuronal nicotinic acetylcholine receptors (nAChR) by nicotine has been suggested to protect neurons against a hypoxic insult. The objective this study was examine the nature cell death induced acute hypoxia in rat primary cortical cultures and neuroprotective potential ameliorating these processes. Neuronal 4-h exposure (0.1% O2) apoptotic, as shown TUNEL staining assays monitoring DNA strand breaks caspase-3/7 activity. presence (10 μM) during insult protected subpopulation susceptible neurones damage apoptosis oxygen deprivation. This protective effect prevented 30-min pre-incubation with either 100 nM α-bungarotoxin or 1 μM dihydro-β-erythroidine, but not atropine, suggesting that activation at least two subtypes nAChR, α7 β2* is involved mediating neuroprotection.