Nicotine and amphetamine acutely cross-potentiate their behavioral and neurochemical responses in female Holtzman rats

Jutkiewicz, Emily M.; Nicolazzo, Danielle; Kim, Myung N.; Gnegy, Margaret E.

doi:10.1007/s00213-008-1159-y

Cited by 28 publications

(35 citation statements)

References 52 publications

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“…For example, nicotine exposure in adolescence has been shown to alter the rewarding effect of cocaine in adulthood [27]. Nicotine enhances locomotor activity to cocaine and activates other indirect dopamine agonists [28], [29]. However, these studies mainly focus on certain genes or neurotransmitters, and cannot understand the underlying mechanism from systems biology framework.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of Metabonomic for a Gateway Drug: Nicotine Priming Enhances Behavioral Response to Cocaine with Modification in Energy Metabolism and Neurotransmitter Level

Bu²,

Chen³

et al. 2014

PLoS ONE

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Nicotine, one of the most commonly used drugs, has become a major concern because tobacco serves as a gateway drug and is linked to illicit drug abuse, such as cocaine and marijuana. However, previous studies mainly focused on certain genes or neurotransmitters which have already been known to participate in drug addiction, lacking endogenous metabolic profiling in a global view. To further explore the mechanism by which nicotine modifies the response to cocaine, we developed two conditioned place preference (CPP) models in mice. In threshold dose model, mice were pretreated with nicotine, followed by cocaine treatment at the dose of 2 mg/kg, a threshold dose of cocaine to induce CPP in mice. In high-dose model, mice were only treated with 20 mg/kg cocaine, which induced a significant CPP. 1H nuclear magnetic resonance based on metabonomics was used to investigate metabolic profiles of the nucleus accumbens (NAc) and striatum. We found that nicotine pretreatment dramatically increased CPP induced by 2 mg/kg cocaine, which was similar to 20 mg/kg cocaine-induced CPP. Interestingly, metabolic profiles showed considerable overlap between these two models. These overlapped metabolites mainly included neurotransmitters as well as the molecules participating in energy homeostasis and cellular metabolism. Our results show that the reinforcing effect of nicotine on behavioral response to cocaine may attribute to the modification of some specific metabolites in NAc and striatum, thus creating a favorable metabolic environment for enhancing conditioned rewarding effect of cocaine. Our findings provide an insight into the effect of cigarette smoking on cocaine dependence and the underlying mechanism.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of Metabonomic for a Gateway Drug: Nicotine Priming Enhances Behavioral Response to Cocaine with Modification in Energy Metabolism and Neurotransmitter Level

Bu²,

Chen³

et al. 2014

PLoS ONE

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“…Other behavioral effects associated with the interaction between nicotine and stimulants, such as cross-sensitization (a neurobiological adaptive process that is thought to play a role in the development and maintenance of addiction; [129]) have been demonstrated. These include interactions between nicotine and amphetamine [130], methylphenidate [131], cocaine [132], and METH [133]. Related neurobiological changes have also been noted in rodents pre-exposed to nicotine.…”

Section: Nicotine + Stimulant Interactionsmentioning

confidence: 99%

Interactions between nicotine and drugs of abuse: a review of preclinical findings

Kohut

2016

The American Journal of Drug and Alcohol Abuse

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Polysubstance abuse is common among substance use disorder patients and nicotine is one of the most commonly co-used substances. Epidemiological and clinical laboratory studies suggest that nicotine, when combined with other drugs of abuse, increases intake of one or both substances. This review focuses on the preclinical literature regarding nicotine’s interaction with alcohol, stimulants (i.e., cocaine, amphetamines), opioids (i.e., morphine, heroin) and Δ9-tetrahydrocannabinol (THC). The current understanding of how these various classes of abused drugs may interact with nicotine on behavioral, physiological, and pharmacological indices that may be important in maintaining co-use of one or both substances in human populations are highlighted. Suggestions as to future areas of research and gaps in knowledge are offered.

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“…We previously reported that a single exposure to nicotine sensitizes locomotor responsiveness to other drugs of abuse, including AMPH, cocaine and methamphetamine. As compared to saline, a low dose of nicotine given to rats sensitized subsequent AMPH-induced locomotor behavior and AMPH-stimulated DA efflux in the striatum measured 1 to 4 hours later (Jutkiewicz et al, 2008), demonstrating a rapid sensitization following nicotine pretreatment. Conversely, an acute dose of AMPH rapidly enhanced locomotor behavior and DA efflux in response to nicotine (Jutkiewicz et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

The sensitizing effect of acute nicotine on amphetamine-stimulated behavior and dopamine efflux requires activation of β2 subunit-containing nicotinic acetylcholine receptors and glutamate N-methyl-d-aspartate receptors

et al. 2011

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Nicotine has been demonstrated to enhance the subsequent use of illicit drugs in animals and humans. We previously demonstrated in female, Holtzman rats that one low dose of nicotine will potentiate locomotor activity and dopamine (DA) efflux in response to a subsequent low dose of d-amphetamine (AMPH) given 1-4 hours later. In the present study, we show this also occurs in male rats and characterize the receptors required for the rapid sensitizing effect of nicotine on AMPH-stimulated locomotor behavior and AMPH-induced DA efflux. Pretreatment of male, Holtzman rats with a low dose (0.1 mg/kg, i.p.) of nicotine 2-4 hours before a challenge with AMPH (0.32 mg/kg, i.p.) enhanced locomotor behavior as compared to saline pretreatment. Dihydro-β-erythroidine (DHβE), a relatively selective antagonist at β2 subunit-containing (β2*) nicotinic acetylcholine receptors (nAChR), but not methyllycaconitine (MLA), a relatively selective antagonist at α7 nAChRs, blocked the sensitizing effect of nicotine on AMPH-stimulated locomotor activity. Pretreatment with varenicline, a partial agonist selective for β2* nAChRs, blocked the sensitizing effect of nicotine on AMPH-stimulated locomotor behavior. Nicotine pretreatment sensitized AMPH-induced DA overflow in slices from ventral (nucleus accumbens, NAc), but not dorsal striatum as compared to saline-pretreated rats. Nicotine sensitization of the DA overflow was blocked by DHβE. Pretreatment with the glutamate N-methyl-D-aspartate (NMDA) receptor antagonist (+)-MK801 (0.1 mg/kg, s.c.) 30 min before nicotine blocked sensitization of both locomotion and DA overflow in response to AMPH challenge. These results demonstrate that activation of the β2* nAChRs and NMDA receptors are required for the rapid sensitizing effect of nicotine on AMPH actions.

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Nicotine and amphetamine acutely cross-potentiate their behavioral and neurochemical responses in female Holtzman rats

Abstract: Overall, the present data demonstrate that acute interactions of nicotine and other psychomotor stimulants produce potentiative effects and that these transient interactions may play a role in the frequent co-use and abuse of nicotine and other stimulants.

Cited by 28 publications

References 52 publications

Mechanisms of Metabonomic for a Gateway Drug: Nicotine Priming Enhances Behavioral Response to Cocaine with Modification in Energy Metabolism and Neurotransmitter Level

Mechanisms of Metabonomic for a Gateway Drug: Nicotine Priming Enhances Behavioral Response to Cocaine with Modification in Energy Metabolism and Neurotransmitter Level

Interactions between nicotine and drugs of abuse: a review of preclinical findings

The sensitizing effect of acute nicotine on amphetamine-stimulated behavior and dopamine efflux requires activation of β2 subunit-containing nicotinic acetylcholine receptors and glutamate N-methyl-d-aspartate receptors

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