Modulation of ethanol drinking-in-the-dark by mecamylamine and nicotinic acetylcholine receptor agonists in C57BL/6J mice.
Modulation of ethanol drinking-in-the-dark by mecamylamine and nicotinic acetylcholine receptor agonists in C57BL/6J mice.
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DOI：
10.1007/s00213-009-1488-5
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发表时间：
2009-07
影响因子：
3.4
通讯作者：
Tapper, Andrew R.
中科院分区：
文献类型：
--
作者：
Hendrickson, Linzy M.;Zhao-Shea, Rubing;Tapper, Andrew R.
最近的报告描述了一种限制性乙醇消耗范例，其中 C57Bl/6J 小鼠饮酒直至中毒。这种范式被称为“黑暗中饮酒”（DID），已被用作酗酒的模型。尽管神经元烟碱乙酰胆碱受体（nAChR）与经过预先训练的自我摄入乙醇的大鼠的饮酒有关，但它们在狂饮型乙醇消耗中的作用尚不清楚。通过 C57Bl/6J 小鼠中的 DID 测定来确定 nAChR 是否与酗酒有关。成年雄性 C57Bl/6J 小鼠腹膜内注射。与烟碱受体拮抗剂一起使用，包括美加明、六甲铵、二氢-β赤霉素和甲基利卡乌丁。注射后立即在 DID 测定中向小鼠提供 20% 乙醇 2 小时以测量乙醇消耗量。还评估了包括金雀花碱和尼古丁在内的烟碱激动剂。通过免疫组织化学评估美加明和尼古丁对乙醇诱导的 VTA 多巴胺能神经元激活的影响。美加明剂量依赖性地减少乙醇消耗；而外周拮抗剂六甲铵则无明显作用。烟碱激动剂金雀花碱和尼古丁减少了乙醇消耗。没有一种有效的烟碱受体药物可以减少蔗糖摄入。美加明阻断了多巴胺能神经元的乙醇激活，而单独的尼古丁则无需乙醇的额外激活即可激活它们。神经元 nAChR 参与 DID 范式中的乙醇消耗。美加明、尼古丁和金雀花碱对乙醇摄入量的影响似乎是特定的，因为它们不会减少蔗糖的饮用。美加明通过阻断多巴胺能神经元的激活来减少饮酒量；而烟碱激动剂可能会激活与酒精相同的奖赏途径。
Recent reports describe a restricted access ethanol consumption paradigm where C57Bl/6J mice drink until intoxicated. Termed “drinking in the dark” (DID), this paradigm has been used as a model of binge drinking. Although neuronal nicotinic acetylcholine receptors (nAChRs) have been implicated in alcohol drinking in rats pre-trained to self-administer ethanol, their role in binge-like ethanol consumption is unknown. To determine if nAChRs are involved in binge drinking as measured by the DID assay in C57Bl/6J mice. Adult male C57Bl/6J mice were injected i.p. with nicotinic receptor antagonists including mecamylamine, hexamethonium, dihydro-β erythroidine, and methyllycaconitine. Immediately following injection mice were presented with 20 % ethanol for 2 hours in the DID assay to measure ethanol consumption. Nicotinic agonists including cytisine and nicotine were also evaluated. The effects of mecamylamine and nicotine on ethanol-induced dopaminergic neuronal activation in the VTA were evaluated via immunohistochemistry. Mecamylamine dose dependently reduced ethanol consumption; whereas the peripheral antagonist hexamethonium had no significant effect. Nicotinic agonists cytisine and nicotine reduced ethanol consumption. None of the effective nicotinic receptor drugs reduced sucrose drinking. Mecamylamine blocked ethanol activation of dopaminergic neurons while nicotine alone activated them without additional activation by ethanol. Neuronal nAChRs are involved in ethanol consumption in the DID paradigm. The effects of mecamylamine, nicotine, and cytisine on ethanol intake appear to be specific because they do not reduce sucrose drinking. Mecamylamine reduces alcohol consumption by blocking activation of dopaminergic neurons; whereas nicotinic agonists may activate the same reward pathway as alcohol.
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DOI：
10.1111/j.1530-0277.2000.tb02104.x
发表时间：
2000-09-01
影响因子：
3.2
作者：
Forman, SA;Zhou, Q
通讯作者：
Zhou, Q
影响因子：
2.5
作者：
ODELL, TJ;CHRISTENSEN, BN
通讯作者：
CHRISTENSEN, BN
影响因子：
5
作者：
Ericson, M;Molander, A;Söderpalm, B
通讯作者：
Söderpalm, B
影响因子：
5
作者：
Blomqvist, O;Ericson, M;Soderpalm, B
通讯作者：
Soderpalm, B
影响因子：
5
作者：
BLOMQVIST, O;ENGEL, JA;SODERPALM, B
通讯作者：
SODERPALM, B