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Titlebook: Effects of Nicotine on Biological Systems II; Paul Brian Sydenham Clarke,Maryka Quik,Klaus Thura Book 1995 Springer Science+Business Media

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樓主: 短暫
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發(fā)表于 2025-3-23 11:53:17 | 只看該作者
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發(fā)表于 2025-3-23 15:18:28 | 只看該作者
Regulation of Neuronal Nicotinic Receptors in Primary Cultures 7 days increases the number of nicotinic receptor binding sites labeled by [.H]cytisine. Primary neuronal cultures should be useful as model systems for studies of subunit composition and molecular mechanisms involved in the regulation of neuronal nicotinic receptors.
13#
發(fā)表于 2025-3-23 20:40:08 | 只看該作者
Conditioned Tolerance to Nicotine in Ratsng mechanisms. Our laboratory is engaged in studies of sensitization (1) and tolerance (2–5) to several therapeutic and addictive drugs. Here we will discuss research on tolerance to intermittent nicotine exposure suggesting that learning plays an important role in its development and manifestation.
14#
發(fā)表于 2025-3-23 23:08:36 | 只看該作者
Involvement of Nicotine and Its Metabolites in the Pathology of Smoking-Related Diseases: Facts and ht be the causative agents remain to be identified. At present, there is no evidence at all that nicotine — the substance most smokers smoke for — has any influence on the development of cancer in otherwise healthy smokers, and only spurious evidence that it may be involved in the development of coronary heart disease.
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發(fā)表于 2025-3-24 06:11:55 | 只看該作者
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發(fā)表于 2025-3-24 11:37:39 | 只看該作者
https://doi.org/10.1007/978-981-15-2282-6of such a requirement, and that the muscle receptor non-alpha subunits relieve the α7 receptor from this requirement. We conclude that cyclophilin might be uniquely required as a PPIase or a molecular chaperone in the folding and assembly of α7 homo-oligomers.
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發(fā)表于 2025-3-24 17:52:46 | 只看該作者
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發(fā)表于 2025-3-24 20:09:19 | 只看該作者
20#
發(fā)表于 2025-3-24 23:36:02 | 只看該作者
https://doi.org/10.1007/978-1-4842-4540-8oline as a neurotrophic factor, but because exogenous drug administration elicits the trophic effect prematurely, neural cell replication is arrested at the incorrect time, leading to deficiencies in cell number and synaptic function.
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