Characteristics of conditioned taste aversion produced by nicotine in rats

Kumar, Ramesh; Pratt, Julian; Stolerman, Ian P.

doi:10.1111/j.1476-5381.1983.tb10518.x

Cited by 87 publications

(34 citation statements)

References 20 publications

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“…Domino 1973;Stolerman et al 1973a;Tripathi et al 1982). Consistent with receptor mediation, stereoselective behavioural actions of nicotine have been reported (Meltzer et al 1980;Clarke and Kumar 1983c;Kumar et al 1983;Garcha et al 1986). Ganglionic (C6) receptors in the CNS may mediate the reinforcing effects of nicotine and tobacco smoke (Stolerman et al 1973b;Hanson et al 1979;Tennant et al 1983).…”

Section: Central Nicotinic Receptor Subtypessupporting

confidence: 49%

Nicotine and smoking: a perspective from animal studies

Clarke

1987

Psychopharmacology

131

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Nicotine plays a key role in reinforcing tobacco smoking, and exerts several psychoneuropharmacological actions which may contribute to its reinforcing effects. Thus, nicotine can improve mood and alleviate withdrawal symptoms; it can also alter CNS arousal, reduce stress, suppress appetite, and improve performance on certain tasks. Behavioural studies in animals have tended to corroborate existing theories of smoking behaviour, and have started to suggest how and where nicotine may exert its central actions in man. Clinical evidence suggests that smoking cessation would be facilitated by the administration of a nicotinic antagonist having a selective action on central nicotinic cholinoceptors of the C6 (ganglionic) type. Pharmacological studies in animals indicate that such a drug is a reasonable prospect.

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Section: Central Nicotinic Receptor Subtypessupporting

confidence: 49%

Nicotine and smoking: a perspective from animal studies

Clarke

1987

Psychopharmacology

131

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“…These results support previous evidence that nicotine can elicit a CTA in rats [Kumar et al, 1983;Stolerman, 1988;Shoaib and Stolerman, 1995]. Moreover, the ability of nicotine to produce a CTA in rats can be blocked by pre-exposure to nicotine in experimentally naive rats or in rats previously trained and tested in a nicotine drug discrimination study.…”

Section: Discussionsupporting

confidence: 87%

“…Systemic administration of nicotine immediately after a session where rodents consumed a novel tasting substance (e.g., saccharin) produces a reduction in the amount of saccharin solution consumed during a follow-up session 24 h later [Kumar et al, 1983;Stolerman, 1988;Gommans et al, 2000;Shoaib et al, 2000]. Nicotine-induced CTA also can be blocked by the nonselective nAChR antagonist mecamylamine [Stolerman, 1988] and the competitive antagonist dihydro-b-erythroidine, although not by the a 7 receptor antagonist, methylycaconotine (MLA; Gommans et al, 2000;Shoaib et al, 2000], indicating that the aversive effects of nicotine are mediated by CNS nAChRs, including those implicated in the rewarding effects of nicotine.…”

Section: Introductionmentioning

confidence: 99%

Acute behavioral tolerance to nicotine in the conditioned taste aversion paradigm

Prus

Maxwell

Baker

et al. 2007

Drug Development Research

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Acute behavioral tolerance to nicotine is a well-established phenomenon in animals, although previous drug discrimination studies have suggested that subpopulations of rats may exist that fail to exhibit acute tolerance to nicotine. The present study sought to determine whether these findings might extend to the conditioned taste aversion (CTA) paradigm. In experiment 1, rats were administered 0.8 mg/kg s.c. nicotine or vehicle before a pairing session with saccharin, and then administered either 0.4 mg/kg nicotine or vehicle immediately afterward. Rats treated with vehicle pre-session and then nicotine postsession developed a significant CTA to nicotine, whereas rats treated with 0.8 mg/kg nicotine s.c. pre-session failed to develop a CTA to nicotine. In experiment 2, rats were identified as exhibiting or failing to exhibit acute tolerance to nicotine in a drug discrimination paradigm. Rats that produced acute nicotine tolerance failed to develop a CTA after 24 h, but did so after 48 h, while rats that did not produce nicotine tolerance exhibited CTA after 24 h, but not after 48 h. These findings indicate that acute behavioral tolerance to nicotine extends to its aversion effects. Drug Dev Res 68: [522][523][524][525][526][527][528] 2007

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“…3), and conditioned taste avoidance (Fig. 4) appear not to be mediated solely by nAChRs, as classic nAChR antagonists only attenuate these effects of nicotine (57,93,137,187). Rauhut et al (139) suggested that facilitation of both DA and NE system function may underlie the bupropion-induced increase in nicotine self-administration, based on results that methamphetamine, but not apomorphine or reboxetine, increase nicotine self-administration.…”

Section: Neurochemical Mechanisms Mediating Effects Of Bupropion On Nmentioning

confidence: 98%

Review of the Pharmacology and Clinical Profile of Bupropion, an Antidepressant and Tobacco Use Cessation Agent

et al. 2006

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Bupropion hydrochloride ((±)-2-tert-butylamino)-3¢-chloropropiophenone · HCl) is a nonselective inhibitor of the dopamine transporter (DAT) and the norepinephrine transporter (NET) and is also an antagonist at neuronal nicotinic acetylcholine receptors (nAChRs). In animal models used commonly to screen for antidepressant activity, bupropion shows a positive response. Also using animal models, bupropion has been shown to attenuate nicotine-induced unconditioned behaviors, to share or enhance discriminative stimulus properties of nicotine and to have a complex effect on nicotine self-administration, i.e., low doses augmenting nicotine self-administration and high doses attenuating self-administration. Current studies show that bupropion facilitates the acquisition of nicotine conditioned place preference in rats, further suggesting that bupropion enhances the rewarding properties of nicotine. Bupropion has been shown to attenuate the expression of nicotine withdrawal symptoms in both animal models and human subjects. With respect to relapse, current studies show that bupropion attenuates nicotine-induced reinstatement in rats, but large individual differences are apparent. Clinically, bupropion is used as a treatment for two indications, as an antidepressant, the indication for which it was developed, and as a tobacco use cessation agent. In clinical trials, bupropion is being tested as a candidate treatment for psychostimulant drug abuse, attention-deficit hyperactivity disorder (ADHD) and obesity. Bupropion is available in three bioequivalent oral formulations, immediate release (IR), sustained release (SR), and extended release (XL). Extensive hepatic

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Characteristics of conditioned taste aversion produced by nicotine in rats

Cited by 87 publications

References 20 publications

Nicotine and smoking: a perspective from animal studies

Nicotine and smoking: a perspective from animal studies

Acute behavioral tolerance to nicotine in the conditioned taste aversion paradigm

Review of the Pharmacology and Clinical Profile of Bupropion, an Antidepressant and Tobacco Use Cessation Agent

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