Early adolescent nicotine exposure affects later-life cocaine reward in mice

Alajaji, Mai; Lazenka, Matthew F.; Kota, Dena; Wise, Laura E.; Younis, Rabha M.; Carroll, F. Ivy; Levine, Amir; Selley, Dana E.; Sim‐Selley, Laura J.; Damaj, M. Imad

doi:10.1016/j.neuropharm.2016.01.032

Cited by 35 publications

(33 citation statements)

References 44 publications

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“…and nicotine (0.5mg/kg; s.c.) were produced after 3 days of conditioning in mice [ F (2, 22) = 57.40, p <0.0001]. The 10 mg/kg dose of cocaine has been previously shown to produce a significant preference in the CPP test (Alajaji et al, 2016; Ignatowska-Jankowska et al, 2013). Although WY-14643, with a 15 min pretreatment, totally reduced nicotine reward at 1mg/kg as previously observed in this study[ F (3, 25) = 21.18, p <0.0001], it had no significant effect on cocaine preference ( p >0.05).…”

Section: Resultsmentioning

confidence: 99%

In vivo interactions between α7 nicotinic acetylcholine receptor and nuclear peroxisome proliferator-activated receptor-α: Implication for nicotine dependence

et al. 2017

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Chronic tobacco use dramatically increases health burdens and financial costs. Limitations of current smoking cessation therapies indicate the need for improved molecular targets. The main addictive component of tobacco, nicotine, exerts its dependency effects via nicotinic acetylcholine receptors (nAChRs). Activation of the homomeric α7 nAChR reduces nicotine's rewarding properties in conditioned place preference (CPP) test and i.v. self-administration models, but the mechanism underlying these effects is unknown. Recently, the nuclear receptor peroxisome proliferator-activated receptor type-α (PPARα) has been implicated as a downstream signaling target of the α7 nAChR in ventral tegmental area dopamine cells. The present study investigated PPARα as a possible mediator of the effect of α7 nAChR activation in nicotine dependence. Our results demonstrate the PPARα antagonist GW6471 blocks actions of the α7 nAChR agonist PNU282987 on nicotine reward in an unbiased CPP test in male ICR adult mice. These findings suggests that α7 nAChR activation attenuates nicotine CPP in a PPARα-dependent manner. To evaluate PPARα activation in nicotine dependence we used the selective and potent PPARα agonist, WY-14643 and the clinically used PPARα activator, fenofibrate, in nicotine CPP and we observed attenuation of nicotine preference, but fenofibrate was less potent. We also studied PPARα in nicotine dependence by evaluating its activation in nicotine withdrawal. WY-14643 reversed nicotine withdrawal signs whereas fenofibrate had modest efficacy. This suggests that PPARα plays a role in nicotine reward and withdrawal and that further studies are warranted to elucidate its function in mediating the effects of α7 nAChRs in nicotine dependence.

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Section: Resultsmentioning

confidence: 99%

In vivo interactions between α7 nicotinic acetylcholine receptor and nuclear peroxisome proliferator-activated receptor-α: Implication for nicotine dependence

et al. 2017

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“…A recent study in mice has also demonstrated long-lasting effects of early adolescent (P28–34) nicotine treatment on psychostimulant reward in adulthood, with nicotine-exposed animals displaying enhanced cocaine and amphetamine conditioned place preference. The same nicotine exposure during late adolescence (P47–59) or adulthood had no effect on subsequent psychostimulant reward (186). …”

Section: Concurrent Use Of Nicotine and Psychostimulantsmentioning

confidence: 99%

Mechanisms and genetic factors underlying co-use of nicotine and alcohol or other drugs of abuse

Cross

Lotfipour

Leslie

2016

The American Journal of Drug and Alcohol Abuse

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Concurrent use of tobacco and alcohol or psychostimulants represents a major public health concern, with use of one substance influencing consumption of the other. Co-abuse of these drugs leads to substantial negative health outcomes, reduced cessation, and high economic costs, but the underlying mechanisms are poorly understood. Epidemiological data suggest that tobacco use during adolescence plays a particularly significant role. Adolescence is a sensitive period of development marked by major neurobiological maturation of brain regions critical for reward processing, learning and memory, and executive function. Nicotine exposure during this time produces a unique and long-lasting vulnerability to subsequent substance use, likely via actions at cholinergic, dopaminergic, and serotonergic systems. In this review, we discuss recent clinical and preclinical data examining the genetic factors and mechanisms underlying co-use of nicotine and alcohol or cocaine and amphetamines. We evaluate the critical role of nicotinic acetylcholine receptors throughout, and emphasize the dearth of preclinical studies assessing concurrent drug exposure. We stress important age and sex differences in drug responses, and highlight a brief, low-dose nicotine exposure paradigm that may better model early use of tobacco products. The escalating use of e-cigarettes among youth necessitates a closer look at the consequences of early adolescent nicotine exposure on subsequent alcohol and drug abuse.

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“…20 Specifically, adult rodents exposed to nicotine as adolescents show a persistent increase in deltaFosB in the nucleus accumbens, impaired GABA signaling in the ventral tegmental area, and changes in brain morphology and gene expression in reward regions. 93,101,[103][104][105] Furthermore, adult rodents exposed to nicotine as adolescents have an increased preference for cocaine, amphetamine, opioids, and higher doses of nicotine. 103 The following section reviews in greater detail the impacts of adolescent versus adult nicotine exposure on subsequent drug use in animal models.…”

Section: Nicotine Uniquely Activates the Adolescent Brain Reward Systemmentioning

confidence: 99%

“…93,101,[103][104][105] Furthermore, adult rodents exposed to nicotine as adolescents have an increased preference for cocaine, amphetamine, opioids, and higher doses of nicotine. 103 The following section reviews in greater detail the impacts of adolescent versus adult nicotine exposure on subsequent drug use in animal models. Other drug-associated behaviors are beyond the scope of this review and will not be discussed.…”

Section: Nicotine Uniquely Activates the Adolescent Brain Reward Systemmentioning

confidence: 99%

“…Chronic nicotine exposure differentially alters cocaine-induced locomotor activity and intravenous cocaine self-administration in adolescent versus adult rodents. 103,[114][115][116] Adolescent rats exposed to nicotine become considerably more sensitized to the locomotor-activating effects of cocaine compared to nonexposed adolescents. 115 Nicotine exposure during adolescence, but not adulthood, also encourages increased self-administration of cocaine during adulthood, suggesting that nicotine use may carry a greater risk during adolescence than adulthood.…”

Section: Adolescent Nicotine Exposure Increases Psychostimulant Reinfmentioning

confidence: 99%

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Nicotine Gateway Effects on Adolescent Substance Use

Ren

Lotfipour

2019

WestJEM

107

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Given the rise in teenage use of electronic nicotine delivery systems ("vaping") in congruence with the increasing numbers of drug-related emergencies, it is critical to expand the knowledge of the physical and behavioral risks associated with developmental nicotine exposure. A further understanding of the molecular and neurochemical underpinnings of nicotine's gateway effects allows emergency clinicians to advise patients and families and adjust treatment accordingly, which may minimize the use of tobacco, nicotine, and future substances. Currently, the growing use of tobacco products and electronic cigarettes among teenagers represents a major public health concern. Adolescent exposure to tobacco or nicotine can lead to subsequent abuse of nicotine and other substances, which is known as the gateway hypothesis. Adolescence is a developmentally sensitive time period when risktaking behaviors, such as sensation seeking and drug experimentation, often begin. These hallmark behaviors of adolescence are largely due to maturational changes in the brain. The developing brain is particularly vulnerable to the harmful effects of drugs of abuse, including tobacco and nicotine products, which activate nicotinic acetylcholine receptors (nAChRs). Disruption of nAChR development with early nicotine use may influence the function and pharmacology of the receptor subunits and alter the release of reward-related neurotransmitters, including acetylcholine, dopamine, GABA, serotonin, and glutamate. In this review, we emphasize that the effects of nicotine are highly dependent on timing of exposure, with a dynamic interaction of nAChRs with dopaminergic, endocannabinoid, and opioidergic systems to enhance general drug reward and reinforcement. We analyzed available literature regarding adolescent substance use and nicotine's impact on the developing brain and behavior using the electronic databases of PubMed and Google Scholar for articles published in English between January 1968 and November 2018. We present a large collection of clinical and preclinical evidence that adolescent nicotine exposure influences long-term molecular, biochemical, and functional changes in the brain that encourage subsequent drug abuse. [West J Emerg Med. 2019;20(5)696-709.] examined in a recent study (2015), which reported that 38.8 percent of adolescents initiate nicotine before alcohol and/ or marijuana, while 21.3 percent use alcohol prior to nicotine and/or marijuana, and 8.6 percent use marijuana before nicotine and/or alcohol. 23 Although previous reports highlight that the rates of cigarette smoking are decreasing in the United States (U.S.), from 20.9 percent in 2005 to 15.5 percent in 2016, current trends in teen use of electronic nicotine delivery systems (e.g., e-cigarettes, vaporizers, hookah pens) are rapidly increasing. 24-26 In particular, the rate of current e-cigarette use in high school students jumped from 1.5 percent in 2011

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Early adolescent nicotine exposure affects later-life cocaine reward in mice

Cited by 35 publications

References 44 publications

In vivo interactions between α7 nicotinic acetylcholine receptor and nuclear peroxisome proliferator-activated receptor-α: Implication for nicotine dependence

In vivo interactions between α7 nicotinic acetylcholine receptor and nuclear peroxisome proliferator-activated receptor-α: Implication for nicotine dependence

Mechanisms and genetic factors underlying co-use of nicotine and alcohol or other drugs of abuse

Nicotine Gateway Effects on Adolescent Substance Use

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