Nicotine-induced conditioned place preference and conditioned place aversion in mice

Risinger, Fred O.; Oakes, Roger A.

doi:10.1016/0091-3057(95)00007-j

Cited by 121 publications

(86 citation statements)

References 21 publications

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“…The administration of higher (1 mg/kg) or lower (0.25 mg/kg) doses of nicotine was ineffective in both genotypes, which excludes a possible shift of the dose-response curve of nicotine in preproenkephalin knock-out mice. In agreement, nicotineinduced conditioned place preference has also been reported previously in rodents (Risinger and Oakes, 1995;Berrendero et al, 2002;Castañé et al, 2002) but only under a narrow range of doses when systemically administered. Indeed, similar ineffective (0.25 and 1 mg/kg) and effective (0.5 mg/kg) doses of nicotine have been reported previously in the mouse place-conditioning paradigm (Risinger and Oakes, 1995;Berrendero et al, 2002;Castañé et al, 2002).…”

Section: Discussionsupporting

confidence: 72%

Nicotine-Induced Antinociception, Rewarding Effects, and Physical Dependence Are Decreased in Mice Lacking the Preproenkephalin Gene

Berrendero¹,

Mendizábal²,

Robledo³

et al. 2005

J. Neurosci.

127

119

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It has been shown previously that the endogenous opioid system may be involved in the behavioral effects of nicotine. In the present study, the participation of endogenous enkephalins on nicotine responses has been investigated by using preproenkephalin knock-out mice. Acute nicotine-induced hypolocomotion remained unaffected in these mice. In contrast, antinociception elicited in the tailimmersion and hot-plate tests by acute nicotine administration was reduced in mutant animals. The rewarding properties of nicotine were then investigated using the place-conditioning paradigm. Nicotine induced a conditioned place preference in wild-type animals, but this effect was absent in knock-out mice. Accordingly, in vivo microdialysis studies revealed that the enhancement in dopamine extracellular levels in the nucleus accumbens induced by nicotine was also reduced in preproenkephalin-deficient mice. Finally, the somatic expression of the nicotine withdrawal syndrome precipitated in nicotine-dependent mice by mecamylamine was significantly attenuated in mutant animals. In summary, the present results indicate that endogenous opioid peptides derived from preproenkephalin are involved in the antinociceptive and rewarding properties of nicotine and participate in the expression of physical nicotine dependence.

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Section: Discussionsupporting

confidence: 72%

Nicotine-Induced Antinociception, Rewarding Effects, and Physical Dependence Are Decreased in Mice Lacking the Preproenkephalin Gene

Berrendero¹,

Mendizábal²,

Robledo³

et al. 2005

J. Neurosci.

127

119

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“…Thus, intermediate doses are effective, low doses are ineffective, and high doses are ineffective or even aversive (Risinger and Oakes, 1995). Nicotine did not induce rewarding effects in any genotype at the dose of 1 mg/kg, but it produced a clear place preference in wild-type mice when administered at the dose of 0.5 mg/kg, as reported previously (Risinger and Oakes, 1995;Castañé et al, 2002). At the dose of 0.7 mg/kg, nicotine also induced rewarding effects in wild-type animals.…”

Section: Discussionmentioning

confidence: 99%

Attenuation of Nicotine-Induced Antinociception, Rewarding Effects, and Dependence in μ-Opioid Receptor Knock-Out Mice

2002

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The involvement of -opioid receptors in different behavioral responses elicited by nicotine was explored by using -opioid receptor knock-out mice. The acute antinociceptive responses induced by nicotine in the tail-immersion and hot-plate tests were reduced in the mutant mice, whereas no difference between genotypes was observed in the locomotor responses. The rewarding effects induced by nicotine were then investigated using the conditioning place-preference paradigm. Nicotine produced rewarding responses in wild-type mice but failed to produce place preference in knock-out mice, indicating the inability of this drug to induce rewarding effects in the absence of -opioid receptors. Finally, the somatic expression of the nicotine withdrawal syndrome, precipitated in dependent mice by the injection of mecamylamine, was evaluated. Nicotine withdrawal was significantly attenuated in knock-out mutants when compared with wild-type mice. In summary, the present results show that -opioid receptors are involved in the rewarding responses induced by nicotine and participate in its antinociceptive responses and the expression of nicotine physical dependence.

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“…Similar to other drugs of abuse, nicotine increases dopamine (DA) release in the nucleus accumbens, and the effects of nicotine on the mesolimbic dopaminergic pathway is thought to mediate the rewarding properties of nicotine [42]. Several behavioral paradigms, such as nicotine self-administration and nicotine conditioned place preference (CPP) have been used to model the rewarding effects of nicotine in animals [139,155]. In nicotine self-administration studies, rodents learn to respond on a lever for nicotine infusions, or receive oral nicotine in a two bottle choice procedure (nicotine-treated water vs. untreated water), whereas subjects in a nicotine CPP procedure learn to prefer a chamber paired with nicotine administration over another chamber that was paired with saline.…”

Section: Nicotinic Acetylcholine Receptors: Animal Researchmentioning

confidence: 99%

Genetic variability in nicotinic acetylcholine receptors and nicotine addiction: Converging evidence from human and animal research

Portugal

Gould

2008

Behavioural Brain Research

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Tobacco smoking is a leading preventable cause of death in the United States and produces a major health and economic burden. Although the majority of smokers want to quit, few are successful. These data highlight the need for additional research into the neurobiology of tobacco dependence. Addiction to nicotine, the main psychoactive component of tobacco, is influenced by multiple factors that include individual differences in genetic makeup. Twin studies have demonstrated that genetic factors can influence vulnerability to nicotine addiction, and subsequent research has identified genes that may alter sensitivity to nicotine. In humans, genome-wide and candidate gene association studies have demonstrated that genes encoding nicotinic acetylcholine receptor (nAChR) proteins are associated with multiple smoking phenotypes. Similarly, research in mice has provided evidence that naturally occurring variability in nAChR genes is associated with changes in nicotine sensitivity. Furthermore, the use of genetic knockout mice has allowed researchers to determine the nAChR genes that mediate the effects of nicotine, whereas research with knockin mice has demonstrated that changes to nAChR genes can dramatically alter nicotine sensitivity. This review will examine the genetic factors that alter susceptibility to nicotine addiction, with an emphasis on the genes that encode nAChR proteins.

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Nicotine-induced conditioned place preference and conditioned place aversion in mice

Cited by 121 publications

References 21 publications

Nicotine-Induced Antinociception, Rewarding Effects, and Physical Dependence Are Decreased in Mice Lacking the Preproenkephalin Gene

Nicotine-Induced Antinociception, Rewarding Effects, and Physical Dependence Are Decreased in Mice Lacking the Preproenkephalin Gene

Attenuation of Nicotine-Induced Antinociception, Rewarding Effects, and Dependence in μ-Opioid Receptor Knock-Out Mice

Genetic variability in nicotinic acetylcholine receptors and nicotine addiction: Converging evidence from human and animal research

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