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• W2001036657 abstract "We previously showed that T- and B-lymphocytes express both muscarinic and nicotinic acetylcholine (ACh) receptors (mAChR and nAChR, respectively), and that stimulation of M(3) mAChRs on lymphocytes increases the intracellular free Ca(2+) concentration ([Ca(2+)](i)) and up-regulates c-fos gene expression. Little is known about the effects of nicotinic stimulation on lymphocyte function, however. We therefore investigated the acute effect of nicotine on [Ca(2+)](i) in CEM cells, a model of T-lymphocytes, using confocal laser scanning microscopy with fluo-3, a Ca(2+)-sensitive fluorescent indicator. In addition, we examined the long-term effect of nicotine on the expression of selected nAChR subunits using semiquantitative reverse transcription-polymerase chain reaction analysis. In the presence of extracellular Ca(2+), nicotine (30 microM) evoked rapid, transient increases in [Ca(2+)](i). This effect was concentration-dependently inhibited by the alpha7 nAChR subunit antagonists, alpha-bungarotoxin (0.01-10 microM) and methyllycaconitine (0.01-10 mM), suggesting that the alpha7 nAChR subunit mediates Ca(2+) signaling in T-lymphocytes. Nicotine (0.01-10 microM) also concentration-dependently down-regulated expression of mRNAs for all the nAChR subunits tested: expression of the alpha6 and alpha7 subunits was down-regulated within 1 week, while expression of the alpha3 and alpha5 subunits declined gradually throughout the 8-week experimental period. These findings indicate that nicotine--and therefore likely smoking--affects immune function by suppressing expression of the neuronal nAChR subtype involved in Ca(2+) signaling in lymphocytes." @default.
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• W2001036657 date "2003-03-01" @default.
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• W2001036657 title "Nicotine-induced Ca2+ signaling and down-regulation of nicotinic acetylcholine receptor subunit expression in the CEM human leukemic T-cell line" @default.
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• W2001036657 doi "https://doi.org/10.1016/s0024-3205(03)00077-8" @default.
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