Tobacco's minor alkaloids: Effects on place conditioning and nucleus accumbens dopamine release in adult and adolescent rats

Marusich, Julie A.; Darna, Mahesh; Wilson, A. George; Denehy, Emily D.; Ebben, Amanda L.; Deaciuc, Agripina G.; Dwoskin, Linda P.; Bardo, Michael T.; Lefever, Timothy W.; Wiley, Jenny L.; Reissig, Chad J.; Jackson, Kia J.

doi:10.1016/j.ejphar.2017.08.029

Cited by 14 publications

(14 citation statements)

References 66 publications

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“…This call profile shift suggests that high-dose nornicotine may be aversive, but whether nornicotine also produces a conditioned place or taste aversion appears unreported. Cotinine is reportedly neutral in the conditioned place preference/aversion assay (Fudala and Iwamoto 1986;Marusich et al 2017), so its lack of effect on call profile (present study) is perhaps to be expected.…”

Section: Effects Of Drugs Alone On Call Rate and Call Profilementioning

confidence: 68%

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Effects of nicotine, nornicotine and cotinine, alone or in combination, on locomotor activity and ultrasonic vocalization emission in adult rats

et al. 2020

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Rationale The behavioral effects of the nicotine metabolites nornicotine and cotinine have not been investigated extensively. Objectives To evaluate the effects of nicotine, cotinine, and nornicotine, given alone or in combination, on locomotor activity and emission of ultrasonic vocalizations in male adult rats. Methods Rats were first given home cage nicotine injections to make them tolerant to the drug's locomotor depressant effects. On subsequent days, locomotor activity (LMA) and ultrasonic vocalizations were recorded in an open field, for 60 min after challenge injection, using repeated measures designs. In single-drug experiments, subjects were tested with nicotine 0.05-0.4 mg/kg, cotinine 0.03-3 mg/kg, or nornicotine 0.1-10 mg/kg. In drug-combination experiments, saline or nicotine 0.2 mg/kg challenge was preceded by cotinine (0, 0.3, 3 mg/kg) or nornicotine (0, 0.1, 0.3, 1, 3 mg/kg) injection. Results High doses of nornicotine increased LMA and blunted the locomotor stimulant effect of nicotine. Less consistently, nicotine and high doses of nornicotine decreased the 50-kHz call rate, with no clear evidence of a nornicotine × nicotine interaction. Cotinine, given alone or before nicotine injection, altered neither LMA nor the call rate. No drug altered the relative prevalence of flat vs. trill 50-kHz call subtypes, except that the highest dose of nornicotine promoted flat calls over trills. No drug evoked 22-kHz calls. Conclusion Nornicotine can exert an acute anti-nicotine effect in vivo, as previously reported in vitro. The finding that nicotine did not detectably alter the 50-kHz call profile appears consistent with this drug's mild subjective effects in human subjects.

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Section: Effects Of Drugs Alone On Call Rate and Call Profilementioning

confidence: 68%

“…Under the same conditions, cotinine did not detectably alter LMA. To our knowledge, acute locomotor effects of cotinine have only been reported in drugnaive rats, with only equivocal signs of locomotor depression (Marusich et al 2017;Wiley et al 2015).…”

Section: Effects Of Drugs Administered Alone On Locomotor Activitymentioning

confidence: 89%

Effects of nicotine, nornicotine and cotinine, alone or in combination, on locomotor activity and ultrasonic vocalization emission in adult rats

et al. 2020

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“…However, baseline dopamine level in tissue samples of NAc and frontal cortex was reported to be comparable between adolescent and adult rats [ 60 ]. Furthermore, nicotine has been shown to increase dopamine release in the NAc in both adults and adolescent rats [ 62 ]. On the other hand, repeated ethanol administration in mice resulted in sensitization only in adults but not adolescents [ 63 ].…”

Section: Discussionmentioning

confidence: 99%

Alterations of Amphetamine Reward by Prior Nicotine and Alcohol Treatment: The Role of Age and Dopamine

2021

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Evidence suggests that nicotine and alcohol can each serve as a gateway drug. We determined whether prior nicotine and alcohol treatment would alter amphetamine reward. Also, we examined whether age and dopaminergic neurotransmission are important in this regard. Male and female adolescent and adult C57BL/6J mice were tested for baseline place preference. Mice then received six conditioning with saline/nicotine (0.25 mg/kg) twice daily, followed by six conditioning with saline/ethanol (2 g/kg). Control mice were conditioned with saline/saline throughout. Finally, mice were conditioned with amphetamine (3 mg/kg), once in the nicotine-alcohol-paired chamber, and tested for place preference 24 h later. The following day, mice were challenged with amphetamine (1 mg/kg) and tested for place preference under a drugged state. Mice were then immediately euthanized, their brain removed, and nucleus accumbens isolated and processed for the level of dopamine receptors and transporter and glutamate receptors. We observed a greater amphetamine-induced place preference in naïve adolescents than adult mice with no change in state-dependent place preference between the two age groups. In contrast, amphetamine induced a significant place preference in adult but not adolescent mice with prior nicotine-alcohol exposure under the drug-free state. The preference was significantly greater in adults than adolescents under the drugged state. The enhanced response was associated with higher dopamine-transporter and D1 but reduced D2 receptors’ expression in adult rather than adolescent mice, with no changes in glutamate receptors levels. These results suggest that prior nicotine and alcohol treatment differentially alters amphetamine reward in adult and adolescent mice. Alterations in dopaminergic neurotransmission may be involved in this phenotype.

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“…This cotinine-mediated dopamine release is blocked by the nicotine receptor antagonists mecamylamine and dihydro-beta-erythroidine (Dwoskin et al, 1999). However, nicotine, but not cotinine, stimulates the release of dopamine in the nucleus accumbens in adolescent and adult rats (Benwell and Balfour, 1992; Marusich et al, 2017). Studies with rodents have shown that nicotine has stimulatory and rewarding effects.…”

Section: Animal Models Of Nicotine Withdrawal Symptomsmentioning

confidence: 99%

Rodent models for nicotine withdrawal

et al. 2021

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Background: Animal models are critical to improve our understanding of the neuronal mechanisms underlying nicotine withdrawal. Nicotine dependence in rodents can be established by repeated nicotine injections, chronic nicotine infusion via osmotic minipumps, oral nicotine intake, tobacco smoke exposure, nicotine vapor exposure, and e-cigarette aerosol exposure. The time course of nicotine withdrawal symptoms associated with these methods has not been reviewed in the literature. Aim: The goal of this review is to discuss nicotine withdrawal symptoms associated with the cessation of nicotine, tobacco smoke, nicotine vapor, and e-cigarette aerosol exposure in rats and mice. Furthermore, age and sex differences in nicotine withdrawal symptoms are reviewed. Results: Cessation of nicotine, tobacco smoke, nicotine vapor, and e-cigarette aerosol exposure leads to nicotine withdrawal symptoms such as somatic withdrawal signs, changes in locomotor activity, anxiety- and depressive-like behavior, learning and memory deficits, attention deficits, hyperalgesia, and dysphoria. These withdrawal symptoms are most pronounced within the first week after cessation of nicotine exposure. Anxiety- and depressive-like behavior, and deficits in learning and memory may persist for several months. Adolescent (4–6 weeks old) rats and mice display fewer nicotine withdrawal symptoms than adults (>8 weeks old). In adult rats and mice, females show fewer nicotine withdrawal symptoms than males. The smoking cessation drugs bupropion and varenicline reduce nicotine withdrawal symptoms in rodents. Conclusion: The nicotine withdrawal symptoms that are observed in rodents are similar to those observed in humans. Tobacco smoke and e-cigarette aerosol contain chemicals and added flavors that enhance the reinforcing properties of nicotine. Therefore, more valid animal models of tobacco and e-cigarette use need to be developed by using tobacco smoke and e-cigarette aerosol exposure methods to induce dependence.

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Tobacco's minor alkaloids: Effects on place conditioning and nucleus accumbens dopamine release in adult and adolescent rats

Cited by 14 publications

References 66 publications

Effects of nicotine, nornicotine and cotinine, alone or in combination, on locomotor activity and ultrasonic vocalization emission in adult rats

Effects of nicotine, nornicotine and cotinine, alone or in combination, on locomotor activity and ultrasonic vocalization emission in adult rats

Alterations of Amphetamine Reward by Prior Nicotine and Alcohol Treatment: The Role of Age and Dopamine

Rodent models for nicotine withdrawal

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