The role of nicotine in smoking: a dual-reinforcement model.

4区 心理学 Q2 Psychology Nebraska Symposium on Motivation Pub Date : 2009-01-01 DOI:10.1007/978-0-387-78748-0_6
Anthony R Caggiula, Eric C Donny, Matthew I Palmatier, Xiu Liu, Nadia Chaudhri, Alan F Sved
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引用次数: 192

Abstract

Models of intravenous nicotine self-administration in laboratory animals are being used to investigate the behavioral and neurobiological consequences of nicotine reinforcement, and to aid in the development of novel pharmacotherapies for smoking cessation. Central to these models is the principle of primary reinforcement, which posits that response-contingent presentation of a primary reinforcer, nicotine, engenders robust operant behavior, whereas response-independent drug delivery does not. This dictum of nicotine as a primary reinforcer has been widely used to explain why people smoke tobacco-smoking results in the rapid delivery of nicotine to the brain, setting up a cascade of neurobiological processes that strengthen subsequent smoking behavior. However, there is mounting evidence that the primary reinforcement model of nicotine self-administration fails to fully explain existing data from both the animal self-administration and human smoking literatures. We have recently proposed a "dual reinforcement" model to more fully capture the relationship between nicotine and self-administration, including smoking. Briefly, the "dual reinforcement" model posits that nicotine acts as both a primary reinforcer and a reinforcement enhancer. The latter action of nicotine had originally been uncovered by showing that a reinforcing VS, which accompanies nicotine delivery, synergizes with nicotine in the acquisition and maintenance of self-administration, and that this synergism can be reproduced by combining operant responding for the reinforcing stimulus with non-contingent (response-independent) nicotine. Thus, self-administration (and smoking) is sustained by three actions: (1) nicotine, acting as a primary reinforcer, can sustain behavior that leads to its delivery; (2) nicotine, acting as a primary reinforcer, can establish neutral environmental stimuli as conditioned reinforcers through Pavlovian associations; and (3) nicotine, acting as a reinforcement enhancer, can magnify the incentive value of accompanying stimuli, be they conditioned or unconditioned reinforcers.

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尼古丁在吸烟中的作用:一个双重强化模型。
实验动物静脉注射尼古丁自我给药模型被用于研究尼古丁强化的行为和神经生物学后果,并有助于开发新的戒烟药物疗法。这些模型的核心是初级强化原理,它假设初级强化物尼古丁的反应偶然呈现会产生稳健的操作行为,而反应独立的药物传递则不会。尼古丁是主要强化物的这一说法被广泛用于解释为什么人们吸烟会导致尼古丁快速传递到大脑,建立一系列神经生物学过程,从而加强随后的吸烟行为。然而,越来越多的证据表明,尼古丁自我给药的初级强化模型不能完全解释动物自我给药和人类吸烟文献中的现有数据。我们最近提出了一个“双重强化”模型,以更全面地捕捉尼古丁与自我给药(包括吸烟)之间的关系。简而言之,“双重强化”模型假定尼古丁既是初级强化剂又是强化增强剂。尼古丁的后一种作用最初是通过表明伴随尼古丁传递的强化VS与尼古丁在获得和维持自我给药过程中协同作用而发现的,并且这种协同作用可以通过将强化刺激的操作性反应与非偶然(反应无关)尼古丁结合来再现。因此,自我给药(和吸烟)是通过三个作用来维持的:(1)尼古丁作为主要的强化物,可以维持导致其传递的行为;(2)尼古丁作为初级强化物,可通过巴甫洛夫联想建立中性环境刺激作为条件强化物;(3)尼古丁作为一种强化增强剂,可以放大伴随刺激的激励价值,无论是条件强化还是非条件强化。
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来源期刊
Nebraska Symposium on Motivation
Nebraska Symposium on Motivation PSYCHOLOGY, SOCIAL-
CiteScore
3.40
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0.00%
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