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首页> 外文期刊>Behavior Genetics >Role of α7- and β4-Containing Nicotinic Acetylcholine Receptors in the Affective and Somatic Aspects of Nicotine Withdrawal: Studies in Knockout Mice
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Role of α7- and β4-Containing Nicotinic Acetylcholine Receptors in the Affective and Somatic Aspects of Nicotine Withdrawal: Studies in Knockout Mice

机译：含有α7和β4的烟碱乙酰胆碱受体在尼古丁戒断的情感和躯体方面的作用：敲除小鼠的研究

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摘要

To assess which nicotinic acetylcholine receptors (nAChRs) are involved in the aversive aspects of nicotine withdrawal, brain reward function and the somatic signs of nicotine withdrawal were assessed in mice that lack α7 and β4 nAChR subunits. Brain reward function was assessed with the intracranial self-stimulation (ICSS) procedure, in which elevations in ICSS thresholds reflect an anhedonic mood state. At 3–6 h of spontaneous nicotine/saline withdrawal, thresholds were elevated in nicotine-withdrawing α7+/+ and β4+/+, but not α7−/− or β4−/−, mice compared with saline-withdrawing mice, indicating a delay in the onset of withdrawal in the knockout mice. From 8 to 100 h of withdrawal, thresholds in α7+/+ and α7−/− mice were equally elevated, whereas thresholds in β4+/+ and β4−/− mice returned to baseline levels. Somatic signs were attenuated in nicotine-withdrawing β4−/−, but not α7−/−, mice. Administration of a low dose of the nAChR antagonist mecamylamine induced threshold elevations in α7−/−, but not α7+/+, mice, whereas the highest dose tested only elevated thresholds in α7+/+ mice. Mecamylamine-induced threshold elevations were similar in β4−/− and β4+/+ mice. In conclusion, null mutation of the α7 and β4 nAChR subunits resulted in a delayed onset of the anhedonic aspects of the spontaneous nicotine withdrawal syndrome. Previous findings of attenuated somatic signs of nicotine withdrawal in β4−/−, but not α7−/−, mice were confirmed in the present study, indicating an important role for β4-containing nAChRs in the somatic signs of nicotine withdrawal. The mecamylamine-precipitated withdrawal data suggest that compensatory adaptations may occur in constitutive α7−/− mice or that mecamylamine may interact with other receptors besides nAChRs in these mice. In summary, the present results indicate an important role for α7 and β4-containing nAChRs in the anhedonic or somatic signs of nicotine withdrawal.
机译：为了评估哪些烟碱乙酰胆碱受体（nAChRs）参与了尼古丁戒断的厌恶方面，在缺乏α7和β4nAChR亚基的小鼠中评估了大脑的奖励功能和尼古丁戒断的体征。通过颅内自我刺激（ICSS）程序评估了大脑奖励功能，其中ICSS阈值的升高反映了无快感状态。在自发戒断尼古丁/盐的3-6小时，戒尼古丁的α7 + / + 和β4 + / + 的阈值升高，但α7- /-或β4-/-小鼠与抽盐水的小鼠相比，表明敲除小鼠的抽搐发作延迟。在戒断的8至100小时内，α7 + / + 和α7-/-小鼠的阈值均升高，而β4 + / + 和β4-/-小鼠恢复到基线水平。抽尼古丁的β4-/-小鼠的体征减弱，但α7-/-小鼠没有。低剂量的nAChR拮抗剂美卡明胺的给药导致α7-/-小鼠的阈值升高，但不引起α7 + / + 小鼠的阈值升高，而测试的最高剂量仅升高了阈值在α7 + / + 小鼠中。在β4-// 和β4 + / + 小鼠中，美卡明胺诱导的阈值升高相似。总之，α7和β4nAChR亚基的无效突变导致自发性尼古丁戒断综合征的性欲减退的延迟发作。先前在β4-/-中发现了尼古丁戒断的体征减​​弱迹象，但在α7-/-中没有发现，这表明β4的重要作用尼古丁戒断的体征中含有nAChRs。美卡敏胺沉淀的戒断数据表明，补偿性适应可能发生在组成型α7-/-小鼠中，或者美卡敏胺可能与这些小鼠中除nAChRs外的其他受体相互作用。总之，目前的结果表明含α7和β4的nAChR在尼古丁戒断的体征或体征中起重要作用。

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