Unique effects of nicotine across the lifespan

Ren, Michelle; Lotfipour, Shahrdad; Leslie, Frances M.

doi:10.1016/j.pbb.2022.173343

Cited by 17 publications

(11 citation statements)

References 143 publications

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“…In addition, baseline and nicotine-induced DA release and nicotine-induced subsequent drug reinforcement (i.e., gateway hypothesis) and acquisition of other drugs of abuse should be assessed in the humanized CHRNA6 3′-UTR SNP rats. Using the 4-day nicotine exposure paradigm, studies have shown nicotine enhances subsequent cocaine [ 36 , 56 , 57 , 58 ], methamphetamine [ 56 , 59 ], ethanol [ 56 ], and fentanyl intake [ 58 , 60 , 61 ]. Furthermore, nicotine potency and efficacy may be shifted in the humanized CHRNA6 3′-UTR SNP rodents, and future studies should implement a dose–response curve.…”

Section: Discussionmentioning

confidence: 99%

Sex- and Genotype-Dependent Nicotine-Induced Behaviors in Adolescent Rats with a Human Polymorphism (rs2304297) in the 3′-UTR of the CHRNA6 Gene

Cardenas

Bai

Heydary

et al. 2022

IJMS

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In human adolescents, a single nucleotide polymorphism (SNP), rs2304297, in the 3′-UTR of the nicotinic receptor subunit gene, CHRNA6, has been associated with increased smoking. To study the effects of the human CHRNA6 3′-UTR SNP, our lab generated knock-in rodent lines with either C or G SNP alleles. The objective of this study was to determine if the CHRNA6 3′-UTR SNP is functional in the knock-in rat lines. We hypothesized that the human CHRNA6 3′-UTR SNP knock-in does not impact baseline but enhances nicotine-induced behaviors. For baseline behaviors, rats underwent food self-administration at escalating schedules of reinforcement followed by a locomotor assay and a series of anxiety tests (postnatal day (PN) 25-39). In separate cohorts, adolescent rats underwent 1- or 4-day nicotine pretreatment (2×, 30 μg/kg/0.1 mL, i.v.). After the last nicotine injection (PN 31), animals were assessed behaviorally in an open-field chamber, and brain tissue was collected. We show the human CHRNA6 3′-UTR SNP knock-in does not affect food reinforcement, locomotor activity, or anxiety. Further, 4-day, but not 1-day, nicotine exposure enhances locomotion and anxiolytic behavior in a genotype- and sex-specific manner. These findings demonstrate that the human CHRNA6 3′-UTR SNP is functional in our in vivo model.

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Section: Discussionmentioning

confidence: 99%

Sex- and Genotype-Dependent Nicotine-Induced Behaviors in Adolescent Rats with a Human Polymorphism (rs2304297) in the 3′-UTR of the CHRNA6 Gene

Cardenas

Bai

Heydary

et al. 2022

IJMS

Self Cite

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“…Animal models suggest that the above association may be due to the unique neurostructural and neurochemical alterations caused by nicotine on the developing adolescent brain [for reviews see (14)(15)(16)(17)]. Briefly, nicotine exposure during adolescence has been shown to (a) cause an extensive upregulation of nicotinic acetylcholine receptors (nAChRs) and reduce the functioning of metabotropic glutamate type 2 receptors (mGluR2) in the PFC, to (b) influence the expression of genes involved in the neuroplasticity of frontal brain regions, and to (c) cause changes in macromolecular constituents indicative of cell loss (reduced DNA) and altered cell size (protein/DNA ratio) in the cerebral cortex, midbrain, and hippocampus of adolescent rodents (17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

Chronic tobacco smoking, impaired reward-based decision-making, and role of insular cortex: A comparison between early-onset smokers and late-onset smokers

Conti

Baldacchino

2022

Front. Psychiatry

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IntroductionThe literature suggests that tobacco smoking may have a neurotoxic effect on the developing adolescent brain. Particularly, it may impair the decision-making process of early-onset smokers (<16 years), by rendering them more prone to impulsive and risky choices toward rewards, and therefore more prone to smoking relapses, in comparison to late-onset smokers (≥16 years). However, no study has ever investigated reward-based decision-making and structural brain differences between early-onset smokers and late-onset smokers.MethodsComputerized measures of reward-based decision-making [Cambridge Gambling Task (CGT); 5-trials adjusting delay discounting task (ADT-5)] were administered to 11 early-onset smokers (mean age at regular smoking initiation = 13.2 years), 17 late-onset smokers (mean age at regular smoking initiation = 18.0 years), and 24 non-smoker controls. Voxel-based morphometry (VBM) was utilized to investigate the gray matter (GM) and white matter (WM) volume differences in fronto-cortical and striatal brain regions between early-onset smokers, late-onset smokers, and non-smokers.ResultsEarly-onset smokers displayed a riskier decision-making behavior in comparison to non-smokers as assessed by the CGT (p < 0.01, Cohen’s f = 0.48). However, no significant differences (p > 0.05) in reward-based decision-making were detected between early-onset smokers and late-onset smokers. VBM results revealed early-onset smokers to present lower GM volume in the bilateral anterior insular cortex (AI) in comparison to late-onset smokers and lower WM volume in the right AI in comparison to late-onset smokers.ConclusionImpairments in reward-based decision-making may not be affected by tobacco smoking initiation during early adolescence. Instead, lower GM and WM volume in the AI of early-onset smokers may underline a vulnerability to develop compulsive tobacco seeking and smoking behavior during adulthood.

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“…Nicotine, a key component found in tobacco and electronic cigarettes, intricately engages with the developing brain primarily through its interaction with nicotinic acetylcholine receptors (nAChRs) crucial for regulating cognitive and neural functions, potentially resulting in changes at both structural and functional levels [ 56 , 57 , 58 ]. Prior research has shown that nicotine exposure during this adolescent and emerging adult developmental phase can influence neural plasticity and neurotransmitter systems, potentially leading to modifications in gray matter integrity, white matter development, and cortical thickness [ 27 , 29 , 59 , 60 , 61 ].…”

Section: Discussionmentioning

confidence: 99%

The Combined Effects of Nicotine and Cannabis on Cortical Thickness Estimates in Adolescents and Emerging Adults

Hernandez Mejia,

Courtney,

Wade

et al. 2024

Brain Sciences

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Early life substance use, including cannabis and nicotine, may result in deleterious effects on the maturation of brain tissue and gray matter cortical development. The current study employed linear regression models to investigate the main and interactive effects of past-year nicotine and cannabis use on gray matter cortical thickness estimates in 11 bilateral independent frontal cortical regions in 223 16–22-year-olds. As the frontal cortex develops throughout late adolescence and young adulthood, this period becomes crucial for studying the impact of substance use on brain structure. The distinct effects of nicotine and cannabis use status on cortical thickness were found bilaterally, as cannabis and nicotine users both had thinner cortices than non-users. Interactions between nicotine and cannabis were also observed, in which cannabis use was associated with thicker cortices for those with a history of nicotine and tobacco product (NTP) use in three left frontal regions. This study sheds light on the intricate relationship between substance use and brain structure, suggesting a potential modulation of cannabis’ impact on cortical thickness by nicotine exposure, and emphasizing the need for further longitudinal research to characterize these interactions and their implications for brain health and development.

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Unique effects of nicotine across the lifespan

Cited by 17 publications

References 143 publications

Sex- and Genotype-Dependent Nicotine-Induced Behaviors in Adolescent Rats with a Human Polymorphism (rs2304297) in the 3′-UTR of the CHRNA6 Gene

Sex- and Genotype-Dependent Nicotine-Induced Behaviors in Adolescent Rats with a Human Polymorphism (rs2304297) in the 3′-UTR of the CHRNA6 Gene

Chronic tobacco smoking, impaired reward-based decision-making, and role of insular cortex: A comparison between early-onset smokers and late-onset smokers

The Combined Effects of Nicotine and Cannabis on Cortical Thickness Estimates in Adolescents and Emerging Adults

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