Abstract

We commend Zernig et al. (2003) for trying to incorporate incentive-sensitization concepts into traditional behavioral pharmacology. However, their present formulation suffers from three crucial misunderstandings. Zernig et al. (2003) said that we “propose that increased drug consumption is not due to tolerance but to sensitization to the drug’s reinforcing effect or ... an increase in drug ‘wanting’”. Then, they presented an alternative explanation. It is difficult to defend a position one never took in the first place, but that is the position we find ourselves. The initial error Zernig et al. (2003) made regarding incentive-sensitization was to say that drug reinforcement roughly corresponds with what we have called drug “wanting”. “Wanting” is a short-hand term for the process of incentive salience attribution, not reinforcement (Robinson and Berridge 1993, 2000, 2003; Berridge and Robinson 1998). To equate reinforcement with “wanting” badly distorts the concept of incentive salience and incentive-sensitization theory. We have said it before and we say it again: drug reinforcement does NOT correspond to drug “wanting”. In our initial paper on this topic (Robinson and Berridge 1993), we included a glossary of terms, including reinforcement, incentive salience and “wanting”. That glossary defined reinforcement in the standard Skinnerian way, as “a purely behavioral and descriptive term for the relationship between the occurrence of a stimulus and changes in the subsequent probability of a behavior” (see p. 281 for the full entry). By contrast, we have consistently defined “wanting” in terms such as, “it is the process of incentive salience attribution that transforms the sensory features of ordinary stimuli or, more accurately, the neural and psychological representations of stimuli, so that they become especially salient stimuli, stimuli that “grab the attention”, that become especially attractive and wanted, thus eliciting approach and guiding behavior to the goal. It is incentive salience that determines the value of incentives” (Robinson and Berridge 2000, p S105). These are obviously very different concepts. We have gone to considerable lengths to distinguish incentive salience from reinforcement, and have pointed out limitations of Skinnerian reinforcement, even arguing that “behaviorist reinforcement should not be mistaken to be an explanation of either drug-taking or addiction in either a physiological or psychological sense” (Robinson and Berridge 2000, p S93; Berridge and Robinson 2003). Zernig et al. (2003) made their second error about incentive-sensitization when they said that we claim incentive-sensitization to be manifest by an upward shift in a cocaine dose–response rate curve. It could be, but we have never said this, because we do not believe an upward shift (or a shift in any direction) in a cocaine dose– response rate curve necessarily indicates sensitization to anything. If anyone else has said it, we think they might misunderstand incentive-sensitization theory. The kinds of dose–response rate functions discussed here are simply the wrong instrument to properly test incentive-sensitization, because they do not specifically measure changes in incentive processes. The rate of drug self-administration is susceptible to influence by too many other processes distinct from incentive salience, such as S-R habit effects, tolerance effects, hedonic effects, cognitive effects, aversive effects, and other effects of drugs. Shifts in dose–response rate functions could be due to changes in any of these processes, making them ambiguous to interpret (Wyvell and Berridge 2000; Berridge and Robinson 2003; Robinson and Berridge 2003). To measure incentive salience separately from other effects, it is necessary to use paradigms that more specifically probe it alone, such as Pavlovian conditioned incentive procedures (e.g., Cardinal 2002; see for discussion Wyvell and Berridge 2000, 2001; Berridge and This reply refers to the letter http://dx.doi.org/10.1007/s00213-0031601-0

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