Nicotine place preference in the mouse: influences of prior handling, dose and strain and attenuation by nicotinic receptor antagonists

Grabus, Sheri D.; Martin, Billy R.; Brown, Sharon E.; Damaj, M. Imad

doi:10.1007/s00213-006-0305-7

Cited by 107 publications

(123 citation statements)

References 43 publications

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“…C57BL/6Ibg mice exhibited greater oral nicotine self-administration than DBA/2Ibg, ST/bJ, BUB/J, A/Ibg, and C3H/2Ibg mice [140]. Furthermore, C57BL/6J mice developed nicotine CPP, whereas DBA/2J mice did not [60]. These data suggest that C57BL/6 mice have increased sensitivity to the rewarding properties of nicotine relative to other strains.…”

Section: The Effects Of Nicotine In Inbred Rodent Strainsmentioning

confidence: 73%

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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Section: The Effects Of Nicotine In Inbred Rodent Strainsmentioning

confidence: 73%

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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“…For acute studies, nicotine solution was adjusted to pH 7.4 with NaOH, and administered subcutaneously (0.5 mg/kg). This dose of nicotine has been shown to induce nicotine CPP in mice (Grabus et al, 2006;Risinger and Oakes, 1995). The 24 mg/ kg/day dose used for chronic nicotine treatments was based on studies that have shown nicotine tolerance as measured by antinociception and withdrawal effects (Matta et al, 2007).…”

Section: Drugsmentioning

confidence: 99%

Reward Sensitization: Effects of Repeated Nicotine Exposure and Withdrawal in Mice

Hilário

Turner

Blendy

2012

Neuropsychopharmacol

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Tobacco dependence is an addiction with high rates of relapse, resulting in multiple quit attempts in individuals who are trying to stop smoking. How these multiple cycles of smoking and withdrawal contribute to nicotine dependence, long-term alterations in brain reward systems, and nicotine receptor regulation is unknown. Therefore, to evaluate how multiple exposures of nicotine and withdrawal periods modulate rewarding properties of nicotine, we used intracranial self-stimulation to measure alterations in the threshold of brain stimulation reward. In addition, we employed the conditioned place preference (CPP) paradigm to evaluate positive context conditioning following each withdrawal period and measured levels of neuronal nicotinic receptors in cortex, striatum, and hippocampus. We found that repeated nicotine exposure and withdrawal enhanced brain stimulation reward and reward sensitivity to acute injections of nicotine. This increased reward was reflected by enhanced CPP to nicotine. Chronic nicotine is known to up-regulate nAChRs (nicotinic acetylcholine receptors) and we found that this up-regulation was maintained for up to 8 days of withdrawal in the striatum and in the hippocampus, but not in the cortex, of animals exposed to multiple nicotine exposure and withdrawal periods. These results demonstrate that repeated exposures to nicotine, followed by withdrawal, induce a persistent increase in both brain reward function and sensitivity to the hedonic value of nicotine and long-lasting up-regulation of neuronal nicotinic receptors. Together, these data suggest that a continuing increase in brain reward function and enhanced sensitivity to nicotine reward following repeated withdrawal periods may be one reason why smokers relapse frequently.

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“…5,[12][13][14] Nicotine, in the absence of tobacco, is sufficient to sustain selfadministration 15 and produce reward in a conditioned place preference paradigm. 16 Nicotine's action requires numerous nAChRs subtypes segregated into high-affinity heteromeric nAChRs containing the β2 subunit (β2*) and low-affinity homomeric α7 nAChRs. 17 They determine the sensitivity of the reward system to a minimum dose of nicotine necessary for VTA DA cell activation and thus nicotine reinforcement.…”

Section: Introductionmentioning

confidence: 99%

Nicotinic receptors mediate stress-nicotine detrimental interplay via dopamine cells’ activity

et al. 2017

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Epidemiological studies report strong association between mood disorders and tobacco addiction. This high comorbidity requires adequate treatment but the underlying mechanisms are unknown. We demonstrate that nicotine exposure, independent of drug withdrawal effects, increases stress sensitivity, a major risk factor in mood disorders. Nicotine and stress concur to induce long-lasting cellular adaptations within the dopamine (DA) system. This interplay is underpinned by marked remodeling of nicotinic systems, causing increased ventral tegmental area (VTA) DA neurons' activity and stress-related behaviors, such as social aversion. Blocking β2 or α7 nicotinic acetylcholine receptors (nAChRs) prevents, respectively, the development and the expression of social stress-induced neuroadaptations; conversely, facilitating α7 nAChRs activation specifically in the VTA promotes stress-induced cellular and behavioral maladaptations. Our work unravels a complex nicotine-stress bidirectional interplay and identifies α7 nAChRs as a promising therapeutic target for stress-related psychiatric disorders.

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Nicotine place preference in the mouse: influences of prior handling, dose and strain and attenuation by nicotinic receptor antagonists

Abstract: Earlier handling experience and strain are important factors when evaluating a nicotine CPP in the mouse. In addition, certain nicotinic receptors underlie the nicotine CPP, indicating that this model can elucidate underlying mediators of nicotine reward.

Cited by 107 publications

References 43 publications

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

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

Reward Sensitization: Effects of Repeated Nicotine Exposure and Withdrawal in Mice

Nicotinic receptors mediate stress-nicotine detrimental interplay via dopamine cells’ activity

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