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安非他酮和尼古丁通过不同的药理学机制增强大鼠对非药物强化物的反应。

Bupropion and nicotine enhance responding for nondrug reinforcers via dissociable pharmacological mechanisms in rats.

机构信息

Department of Psychology, Kansas State University, Manhattan, KS 66502, USA.

出版信息

Psychopharmacology (Berl). 2009 Dec;207(3):381-90. doi: 10.1007/s00213-009-1666-5. Epub 2009 Sep 17.

DOI:10.1007/s00213-009-1666-5
PMID:19760281
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2884399/
Abstract

RATIONALE

Nicotine serves as a primary reinforcer but also potently enhances responding for nonnicotine stimuli with reinforcing properties. One of the most successful pharmacotherapies for smoking cessation, bupropion, also increases responding for nondrug reinforcers such as food and brain stimulation rewards.

OBJECTIVE

The present studies investigated whether treatment with bupropion and nicotine had similar effects on responding for a reinforcing visual stimulus (VS). They also investigated whether the effects of bupropion and nicotine depended on common pharmacological substrates.

RESULTS

Nicotine (0.4 mg/kg base) enhanced responding for the VS, and this enhancing effect increased across testing sessions, replicating our previous findings. Bupropion (3, 10, and 30 mg/kg salt) dose-dependently increased responding for the VS. Treatment with 10 and 30 mg/kg bupropion resulted in a profile similar to nicotine; operant responding increased over repeated drug treatments. The reinforcement enhancing effect of nicotine, but not bupropion, was blocked by pretreatment with the nicotinic acetylcholine receptor antagonist mecamylamine. In contrast, the reinforcement enhancing effect of bupropion, but not nicotine, was blocked by pretreatment with the alpha noradrenergic antagonist prazosin.

CONCLUSION

The reinforcement enhancing effects of nicotine and bupropion increased over time and repeated treatments suggesting a shared mechanism of action. However, the reinforcement enhancing effects of nicotine are mediated by nicotinic acetylcholine receptors, whereas the reinforcement enhancing effects of bupropion were mediated by alpha noradrenergic receptors.

摘要

原理

尼古丁是一种主要的强化物,但也能强烈增强具有强化属性的非尼古丁刺激物的反应。戒烟最成功的药物治疗之一——安非他酮,也会增加对非药物强化物的反应,如食物和大脑刺激奖励。

目的

本研究调查了安非他酮和尼古丁治疗是否对强化视觉刺激(VS)的反应有类似的影响。他们还调查了安非他酮和尼古丁的作用是否依赖于共同的药理学基础。

结果

尼古丁(0.4 毫克/千克碱)增强了对 VS 的反应,这种增强作用在测试过程中逐渐增加,复制了我们之前的发现。安非他酮(3、10 和 30 毫克/千克盐)剂量依赖性地增加了对 VS 的反应。用 10 和 30 毫克/千克安非他酮治疗,结果与尼古丁相似;操作反应随着反复的药物治疗而增加。尼古丁的强化增强作用,但不是安非他酮,被烟碱型乙酰胆碱受体拮抗剂美加明预处理所阻断。相比之下,安非他酮的强化增强作用,但不是尼古丁,被α-去甲肾上腺素能拮抗剂普萘洛尔预处理所阻断。

结论

尼古丁和安非他酮的强化增强作用随着时间的推移和重复治疗而增加,这表明它们具有共同的作用机制。然而,尼古丁的强化增强作用是通过烟碱型乙酰胆碱受体介导的,而安非他酮的强化增强作用是通过α-去甲肾上腺素能受体介导的。

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Chronic bupropion differentially alters the reinforcing, reward-enhancing and conditioned motivational properties of nicotine in rats.
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Bupropion increases activation in nucleus accumbens during anticipation of monetary reward.安非他酮增加了伏隔核在预期金钱奖励时的激活。
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