Nicotinic receptor stimulation protects neurons against beta-amyloidtoxicity
T. Kihara
Bok Engelsk 1997
| Utgitt | 1997
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|---|---|
| Omfang | Side 159- 163
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| Opplysninger | beta-Amyloid (A beta), a major constituent of senile plaques inAlzheimer's disease (AD), is thought to contribute to theneurodegeneration. We examined the effects of nicotinic receptoragonists on AP cytotoxicity in cultured rat cortical neurons. Thenumber of viable neurons decreased significantly when cultures wereexposed to synthetic AP peptides (25-35). Concomitant administrationof nicotine with AP markedly reduced the number of dead cells. Thisnicotine-induced neuroprotection was dependent on the concentration.When hexamethonium or mecamylamine, nicotinic antagonist, was added,neuroprotective effect of nicotine was blocked, which indicates thateffect of nicotine was mediated by nicotinic receptors, In addition,a selective alpha 7-receptor antagonist, cw-bungarotoxin (alpha-BTX),blocked the neuroprotective effect of nicotine. Furthermore,incubation with 3-(2,4)-dimethoxybenzylidene anabaseine (DMXB), aselective alpha 7-receptor agonist, protected against AP-inducedneuronal death. These results suggest that alpha 7-receptoractivation plays an important role in neuroprotection against APcytotoxicity. This study suggests that nicotinic receptorstimulation, especially alpha 7-receptor activation, may be able toprotect neurons from degeneration induced by AP and may have effectsthat counter the progress of AD.
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| Emner |
