Introduction: Cigarette smoking is largely driven by the reinforcing properties of nicotine. Intravenous (IV) self-administration procedures are the gold standard for investigating the rein- forcing effects of psychoactive drugs. The goal of this review was to examine the results of pub- lished investigations of the reinforcing effects of nicotine measured using IV self-administration procedures in humans and nonhuman primates. Results: The body of literature using nonhuman primate subjects indicates nicotine functions as a positive reinforcer when available for self-administration via IV catheters. However, it can also be difficult to establish IV nicotine self-administration in nonhuman primates and sometimes supple - mental strategies have been required (e.g., priming injections or food deprivation) before subjects acquire the behavior. Although the body of literature using human subjects is limited, the evidence indicates nicotine functions as a reinforcer via the IV route of administration in adult cigarette smokers. Rates of nicotine self-injection can be variable across subjects and responding is some- times inconsistent across sessions in both humans and nonhuman primates. Conclusions: The Family Smoking Prevention and Tobacco Control Act, enacted in 2009, gave the Food and Drug Administration regulatory authority over the manufacture, marketing, and distribu- tion of tobacco products. Research examining the threshold reinforcing doses for initiation and maintenance of nicotine self-administration, comparisons of the reinforcing effects of nicotine in adolescent versus adult subjects, investigations of gender differences in the reinforcing effects of nicotine, and studies of the abuse liability of non-nicotine tobacco product constituents and their ability to alter the reinforcing effects of nicotine will inform potential tobacco regulatory actions.

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The Reinforcing Effects of Nicotine in Humans and Nonhuman Primates: A Review of Intravenous Self-Administration Evidence and Future Directions for Research.

Anxiolytic and antidepressant effects of ACPA and harmaline co-treatment.

Heterocyclic aromatic amines induce Neuro-2a cells cytotoxicity through oxidative stress-mediated mitochondria-dependent apoptotic signals.

Effects of adolescent methamphetamine and nicotine exposure on behavioral performance and MAP-2 immunoreactivity in the nucleus accumbens of adolescent mice.

Identifying novel constituents that contribute to tobacco addiction is essential for developing more effective treatments and informing FDA regulation of tobacco products. While preclinical data indicate that monoamine oxidase (MAO) inhibitors can have abuse liability or potentiate the addiction-related effects of nicotine, most of these studies have used clinical MAO inhibitors (e.g., tranylcypromine) that are not present in cigarette smoke. The primary goal of this study was to evaluate the abuse potential of the β-carbolines harmane, norharmane, and harmine - MAO inhibitors that are found in cigarette smoke - in an intracranial self-simulation (ICSS) model in rats. A secondary goal was to evaluate the ability of norharmane to influence nicotine's acute effects on ICSS. None of the β-carbolines lowered ICSS thresholds at any dose studied when administered alone, suggesting a lack of abuse liability. Rather, all three β-carbolines produced dose-dependent elevations in ICSS thresholds, indicating aversive/anhedonic effects. Harmane and harmine also elevated ICSS response latencies, suggesting a disruption of motor function, albeit with reduced potency compared to their ICSS threshold-elevating effects. Norharmane (2.5 mg/kg) modestly attenuated the effects of nicotine on ICSS thresholds. Our findings indicate that these β-carbolines produced only aversive/anhedonic effects in an ICSS model when administered alone, and that norharmane unexpectedly attenuated nicotines acute effects on ICSS. Future work evaluating the addiction-related effects of nicotine combined with these and other MAO inhibitors present in smoke may be useful for understanding the role of MAO inhibition in tobacco addiction and informing FDA tobacco regulation.

β-Carbolines found in cigarette smoke elevate intracranial self-stimulation thresholds in rats.

Effects of adolescent treatment with nicotine, harmane, or norharmane in male Sprague–Dawley rats

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Effects of adolescent treatment with nicotine, harmane, or norharmane in male Sprague–Dawley rats