作者: Henry N Nguyen , Bruce A Rasmussen , David C Perry , None
DOI: 10.1111/J.1471-4159.2004.02482.X
关键词: Chemistry 、 Interpeduncular nucleus 、 Cytisine 、 Epibatidine 、 Cerebral cortex 、 Acetylcholine 、 Stimulation 、 Nicotinic agonist 、 Internal medicine 、 Endocrinology 、 Nicotine
摘要: Chronic nicotine exposure up-regulates neuronal nicotinic receptors, but the functional consequences for these receptors is less well understood. Following 2 weeks of or saline treatment by osmotic minipump, activity was measured concentration-response curves epibatidine-stimulated (86)Rb efflux. Nicotine-treated animals had a significantly higher maximal efflux in cerebral cortex and superior colliculus, not thalamus interpeduncular nucleus plus medial habenula. This increase confirmed separate experiment with stimulation single concentrations epibatidine (cortex, colliculus) (cortex only). did alter stimulated cytisine, an alpha3beta4-selective agonist, potassium chloride, any region. Short-term (16 h) caused no changes either receptor binding [(3)H]epibatidine. Binding increased after cortex, colliculus thalamus, The increases four regions tested linearly correlated [(3)H]epibatidine (R(2) = 0.91), suggesting that rat brain up-regulated chronic are active. These results have important understanding neurobiology smokers users replacement therapy.