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The number of viable neurons decreased significantly when cultures were exposed to synthetic A\u03b2 peptides (25\u201335). Concomitant administration of nicotine with A\u03b2 markedly reduced the number of dead cells. This nicotine\u2010induced neuroprotection was dependent on the concentration. When hexamethonium or mecamylamine, nicotinic antagonist, was added, neuroprotective effect of nicotine was blocked, which indicates that effect of nicotine was mediated by nicotinic receptors. In addition, a selective \u03b17\u2010receptor antagonist, \u03b1\u2010bungarotoxin (\u03b1\u2010BTX), blocked the neuroprotective effect of nicotine. Furthermore, incubation with 3\u2013(2,4)\u2010dimethoxybenzylidene anabaseine (DMXB), a selective \u03b17\u2013receptor agonist, protected against A\u03b2\u2010induced neuronal death. These results suggest that \u03b17\u2013receptor activation plays an important role in neuroprotection against A\u03b2 cytotoxicity. This study suggests that nicotinic receptor stimulation, especially \u03b1\u2010receptor activation, may be able to protect neurons from degeneration induced by A\u03b2 and may have effects that counter the progress of AD.<\/jats:p>","DOI":"10.1002\/ana.410420205","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T15:04:12Z","timestamp":1104591852000},"page":"159-163","source":"Crossref","is-referenced-by-count":279,"title":["Nicotinic receptor stimulation protects neurons against \u03b2\u2010amyloid 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