Effects of Ethanol Exposure During Adolescence or Adulthood on Locomotor Sensitization and Dopamine Levels in the Reward System

Carrara-Nascimento, Priscila Fernandes; Hoffmann, Lucas Barbosa; Flório, Jorge Camilo; Planeta, Cleópatra da Silva; Camarini, Rosana

doi:10.3389/fnbeh.2020.00031

Cited by 15 publications

(18 citation statements)

References 72 publications

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“…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 ]. These authors also showed that adolescent mice exhibited lower dopamine levels in the PFC and NAc following ethanol exposure than adults [ 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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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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“…Furthermore, nicotine has been shown to increase dopamine release in NAc in both adults and adolescent rats (Marusich et al 2017). On the other hand, repeated ethanol administration in mice resulted in sensitization only in the adults, but not adolescents (Carrara-Nascimento et al 2020). These authors also showed that adolescent mice exhibited lower dopamine levels in the PFC and NAc following ethanol exposure, compared to adults (Carrara-Nascimento et al 2020).…”

Section: Discussionmentioning

confidence: 92%

“…On the other hand, repeated ethanol administration in mice resulted in sensitization only in the adults, but not adolescents (Carrara-Nascimento et al 2020). These authors also showed that adolescent mice exhibited lower dopamine levels in the PFC and NAc following ethanol exposure, compared to adults (Carrara-Nascimento et al 2020). Cumulatively, based on the published data, it could be suggested that a greater CPP response following amphetamine in adult mice, observed in our study, could be related to dynamic changes in ethanolinduced decrease in dopamine release in NAc between adolescent and adult mice or a combination of action of nicotine and alcohol pre-exposure.…”

Section: Discussionmentioning

confidence: 96%

Alterations of the rewarding actions of amphetamine by prior nicotine and alcohol treatment: The role of age and dopamine

Stojakovic

Lutfy

2020

Preprint

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RationaleNicotine and alcohol each can serve as the gateway to other drugs.ObjectiveThe current study was sought to determine if prior nicotine and alcohol exposure alters amphetamine reward and if age and dopaminergic neurotransmission are involved.MethodsMale and female adolescent and adult C57BL/6J mice were tested for baseline place preference, received six conditioning with saline/nicotine (0.25 mg/kg) twice daily followed by six conditioning with saline/ethanol (2 g/kg) in a counterbalance manner. 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 then tested for CPP 24 h later. The following day, mice were challenged with amphetamine (1 mg/kg) and tested for CPP under a drugged state. Mice were then immediately euthanized, brain removed and nucleus accumbens isolated and processed for the expression of dopamine receptors and transporter, and glutamate receptors.ResultsWe observed a greater amphetamine-induced CPP in adolescent than adult mice but no change in state-dependent CPP between the two age groups. In contrast, amphetamine-induced CPP in mice with prior nicotine-alcohol exposure was greater in adult than adolescent mice under both drug-free and drugged states. The enhanced response in adult mice was associated with greater expression of dopamine-transporter, reduced D2 receptors, and increased D1 receptors with no changes in glutamate receptors.ConclusionsThese results suggest that prior nicotine and alcohol exposure differentially alters the rewarding action of amphetamine in adult and adolescent mice and alterations in dopaminergic neurotransmission may be involved in this phenotype.

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“…Relatively fewer studies, however, have explored ethanol’s impact on dopamine transmission following adolescent exposure. There is some evidence that adolescent ethanol exposure between postnatal days (PDs) 30 and 45 can decrease accumbal dopamine tissue content in male mice when assessed following five days of abstinence [ 24 ]. Interestingly, intermittent ethanol exposure between PDs 30 and 50, followed by 15 days of abstinence, resulted in elevated basal levels of dopamine in the NAc in adult rats [ 25 ].…”

Section: Introductionmentioning

confidence: 99%

Adolescent Intermittent Ethanol Exposure Effects on Kappa Opioid Receptor Mediated Dopamine Transmission: Sex and Age of Exposure Matter

et al. 2020

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Underage alcohol drinking increases the risk of developing alcohol use disorder (AUD). In rodents, adolescent ethanol exposure augments ethanol consumption and anxiety-like behavior while reducing social interaction. However, the underlying mechanisms driving these adaptations are unclear. The dopamine and kappa opioid receptor (KOR) systems in the nucleus accumbens (NAc) are implicated in affective disorders, including AUD, with studies showing augmented KOR function and reduced dopamine transmission in ethanol-dependent adult animals. Thus, here we examine the impact of adolescent intermittent ethanol (AIE) exposure on dopamine transmission and KOR function in the NAc. Rats were exposed to water or ethanol (4 g/kg, intragastrically) every other day during early (postnatal day (PD) 25–45) or late (PD 45–65) adolescence. While AIE exposure during early adolescence (early-AIE) did not alter dopamine release in male and female rats, AIE exposure during late adolescence (late-AIE) resulted in greater dopamine release in males and lower dopamine release in females. To determine the impact of AIE on KOR function, we measured the effect of KOR activation using U50,488 (0.01–1.00 µM) on dopamine release. Early-AIE exposure potentiated KOR-mediated inhibition of dopamine release in females, while late-AIE exposure attenuated this effect in males. Interestingly, no differences in KOR function were observed in early-AIE exposed males and late-AIE exposed females. Together, these data suggest that AIE exposure impact on neural processes is dependent on sex and exposure timing. These differences likely arise from differential developmental timing in males and females. This is the first study to show changes in KOR function following AIE exposure.

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Effects of Ethanol Exposure During Adolescence or Adulthood on Locomotor Sensitization and Dopamine Levels in the Reward System

Cited by 15 publications

References 72 publications

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

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

Alterations of the rewarding actions of amphetamine by prior nicotine and alcohol treatment: The role of age and dopamine

Adolescent Intermittent Ethanol Exposure Effects on Kappa Opioid Receptor Mediated Dopamine Transmission: Sex and Age of Exposure Matter

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