Effect of Monoamine Oxidase Inhibition on Rewarding Effects of Nicotine in Rodents

Kapelewski, Christine H.; Vandenbergh, David J.; Klein, Laura Cousino

doi:10.2174/1874473711104020110

Cited by 12 publications

(7 citation statements)

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“…The discrepancy between the escalation of smoking behavior in humans (Conklin et al, 2005;Doubeni et al, 2010;Kim et al, 2009) and difficulties demonstrating the escalation of nicotine intake in animals may also reflect the fact that humans do not abuse nicotine, but rather tobacco. Among other chemicals, tobacco smoke contains both MOA-A and MAO-B inhibitors (Kapelewski et al, 2011), resulting in reduced brain MAO activity in smokers (Fowler et al, 1996). Previous studies showed that rodents pretreated daily with mixed irreversible MAO-A and MAO-B inhibitors, such as tranylcypromine (Villégier et al, 2003(Villégier et al, , 2006 and phenelzine (Guillem et al, 2005), exhibited increases in nicotine-induced behaviors, including locomotor activity and limited-access self-administration under both FR and PR schedules of reinforcement.…”

Section: Discussionmentioning

confidence: 99%

Robust Escalation of Nicotine Intake with Extended Access to Nicotine Self-Administration and Intermittent Periods of Abstinence

Cohen

Koob

George

2012

Neuropsychopharmacol

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Although established smokers have a very regular pattern of smoking behavior, converging lines of evidence suggest that the escalation of smoking behavior is a critical factor in the development of dependence. However, the neurobiological mechanisms that underlie the escalation of smoking are unknown, because there is no animal model of the escalation of nicotine intake. On the basis of the pattern of smoking behavior in humans and presence of monoamine oxidase inhibitors in tobacco smoke, we hypothesized that the escalation of nicotine intake may only occur when animals are given extended-access (21 h per day) self-administration sessions after repeated periods of abstinence (24-48 h), and after chronic inhibition of monoamine oxidase using phenelzine sulfate. Intermittent access (every 24-48 h) to extended nicotine self-administration produced a robust escalation of nicotine intake, associated with increased responding under fixed- and progressive-ratio schedules of reinforcement, and increased somatic signs of withdrawal. The escalation of nicotine intake was not observed in rats with intermittent access to limited (1 h per day) nicotine self-administration or daily access to extended (21 h per day) nicotine self-administration. Moreover, inhibition of monoamine oxidase with daily administration of phenelzine increased nicotine intake by ≈ 50%. These results demonstrate that the escalation of nicotine intake only occurs in animals given intermittent periods of abstinence with extended access to nicotine, and that inhibition of monoamine oxidase may contribute to the escalation of smoking, thus validating both an animal model of the escalation of smoking behavior and the contribution of monoamine oxidase inhibition to compulsive nicotine-seeking.

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Section: Discussionmentioning

confidence: 99%

Robust Escalation of Nicotine Intake with Extended Access to Nicotine Self-Administration and Intermittent Periods of Abstinence

Cohen

Koob

George

2012

Neuropsychopharmacol

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“…However, the mixed subjective reports, early difficulties obtaining reliable intravenous nicotine self-administration in animals, and direct comparisons in animal models suggest that the reinforcing efficacy of nicotine is lower than other drugs of abuse (Risner and Goldberg, 1983; Manzardo et al, 2002; Le Foll and Goldberg, 2009). Non-nicotinic aspects of tobacco smoke, such as its other constituents (e.g., acetaldehyde, nornicotine, and harman) and sensory stimulation could substantially contribute to its abuse and addictive potential (Belluzzi et al, 2005; Rose, 2006; Rose et al, 2010; Kapelewski et al, 2011). …”

Section: Features Of Tobacco Smoking Nicotine Abuse and Dependence mentioning

confidence: 99%

Animal Models of Nicotine Exposure: Relevance to Second-Hand Smoking, Electronic Cigarette Use, and Compulsive Smoking

Cohen¹,

George²

2013

Front. Psychiatry

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Much evidence indicates that individuals use tobacco primarily to experience the psychopharmacological properties of nicotine and that a large proportion of smokers eventually become dependent on nicotine. In humans, nicotine acutely produces positive reinforcing effects, including mild euphoria, whereas a nicotine abstinence syndrome with both somatic and affective components is observed after chronic nicotine exposure. Animal models of nicotine self-administration and chronic exposure to nicotine have been critical in unveiling the neurobiological substrates that mediate the acute reinforcing effects of nicotine and emergence of a withdrawal syndrome during abstinence. However, important aspects of the transition from nicotine abuse to nicotine dependence, such as the emergence of increased motivation and compulsive nicotine intake following repeated exposure to the drug, have only recently begun to be modeled in animals. Thus, the neurobiological mechanisms that are involved in these important aspects of nicotine addiction remain largely unknown. In this review, we describe the different animal models available to date and discuss recent advances in animal models of nicotine exposure and nicotine dependence. This review demonstrates that novel animal models of nicotine vapor exposure and escalation of nicotine intake provide a unique opportunity to investigate the neurobiological effects of second-hand nicotine exposure, electronic cigarette use, and the mechanisms that underlie the transition from nicotine use to compulsive nicotine intake.

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“…Also, it is known that women are more likely to experience depressive symptoms during tobacco smoking cessation (36-38), and depression serves as a risk factor for tobacco smoking relapse during abstinence (35, 39). Animal and in vitro studies have suggested that components of tobacco smoke significantly inhibit monoamine oxidase (MAO) (40-42) despite the mixed reports for the effect of nicotine itself (40, 43). Human studies using positron emission tomography have confirmed that tobacco smoke significantly inhibits MAO-A (44, 45), which is known to result in antidepressant-like effects (46).…”

Section: Introductionmentioning

confidence: 99%

Gender differences in the effect of tobacco use on brain phosphocreatine levels in methamphetamine-dependent subjects

Sung

Yurgelun‐Todd

Kondo

et al. 2015

The American Journal of Drug and Alcohol Abuse

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Background A high prevalence of tobacco smoking has been observed in methamphetamine users, but there have been no in vivo brain neurochemistry studies addressing gender effects of tobacco smoking in methamphetamine users. Methamphetamine addiction is associated with increased risk of depression and anxiety in females. There is increasing evidence that selective analogues of nicotine, a principal active component of tobacco smoking, may improve depression and cognitive performance in animals and humans. Objectives To investigate the effects of tobacco smoking and gender on brain phosphocreatine (PCr) levels, a marker of brain energy metabolism reported to be reduced in methamphetamine-dependent subjects. Methods Thirty female and twenty-seven male methamphetamine-dependent subjects were evaluated with phosphorus-31 magnetic resonance spectroscopy (31P-MRS) to measure PCr levels within the pregenual anterior cingulate, which has been implicated in methamphetamine neurotoxicity. Results Analysis of covariance revealed that there were statistically significant slope (PCr versus lifetime amount of tobacco smoking) differences between female and male methamphetamine-dependent subjects (p=0.03). In females, there was also a statistically significant interaction between lifetime amounts of tobacco smoking and methamphetamine in regard to PCr levels (p=0.01), which suggests that tobacco smoking may have a more significant positive impact on brain PCr levels in heavy, as opposed to light to moderate, methamphetamine-dependent females. Conclusion These results indicate that tobacco smoking has gender-specific effects in terms of increased anterior cingulate high energy PCr levels in methamphetamine-dependent subjects. Cigarette smoking in methamphetamine-dependent women, particularly those with heavy methamphetamine use, may have a potentially protective effect upon neuronal metabolism.

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Effect of Monoamine Oxidase Inhibition on Rewarding Effects of Nicotine in Rodents

Cited by 12 publications

References 0 publications

Robust Escalation of Nicotine Intake with Extended Access to Nicotine Self-Administration and Intermittent Periods of Abstinence

Robust Escalation of Nicotine Intake with Extended Access to Nicotine Self-Administration and Intermittent Periods of Abstinence

Animal Models of Nicotine Exposure: Relevance to Second-Hand Smoking, Electronic Cigarette Use, and Compulsive Smoking

Gender differences in the effect of tobacco use on brain phosphocreatine levels in methamphetamine-dependent subjects

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