Genotype-dependent effects of adolescent nicotine exposure on dopamine functional dynamics in the nucleus accumbens shell in male and female mice: a potential mechanism underlying the gateway effect of nicotine

Dickson, Price E.; Rogers, Tiffany D.; Lester, Deranda B.; Miller, Mellessa M.; Matta, Shannon G.; Chesler, Elissa J.; Goldowitz, Dan; Blaha, Charles D.; Mittleman, Guy

doi:10.1007/s00213-010-2159-2

Cited by 20 publications

(16 citation statements)

References 85 publications

(109 reference statements)

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“…The cocaine IVSA testing procedure and chambers have been described in detail previously (Dickson et al 2011). Prior to catheter implantation, mice were housed in same-sex and same-strain groups of 3 to 5.…”

Section: Methodsmentioning

confidence: 99%

Systems genetics of intravenous cocaine self-administration in the BXD recombinant inbred mouse panel

et al. 2015

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Rationale Cocaine addiction is a major public health problem with a substantial genetic basis for which the biological mechanisms remain largely unknown. Systems genetics is a powerful method for discovering novel mechanisms underlying complex traits, and intravenous drug self-administration (IVSA) is the gold standard for assessing volitional drug use in preclinical studies. We have integrated these approaches to identify novel genes and networks underling cocaine use in mice. Methods Mice from 39 BXD strains acquired cocaine IVSA (0.56 mg/kg/infusion). Mice from 29 BXD strains completed a full dose-response curve (0.032 – 1.8 mg/kg/infusion). Results We identified independent genetic correlations between cocaine IVSA and measures of environmental exploration and cocaine sensitization. We identified genome-wide significant QTL on chromosomes 7 and 11 associated with shifts in the dose-response curve and on chromosome 16 associated with sessions to acquire cocaine IVSA. Using publicly available gene expression data from the nucleus accumbens, midbrain, and prefrontal cortex of drug-naïve mice, we identified Aplp1 and Cyfip2 as positional candidates underlying the behavioral QTL on chromosomes 7 and 11, respectively. A genome-wide significant trans-eQTL linking Fam53b (a GWAS candidate for human cocaine dependence) on chromosome 7 to the cocaine IVSA behavioral QTL on chromosome 11 was identified in the midbrain; Fam53b and Cyfip2 were co-expressed genome-wide significantly in the midbrain. This finding indicates that cocaine IVSA studies using mice can identify genes involved in human cocaine use. Conclusions These data provide novel candidate genes underlying cocaine IVSA in mice, and suggest mechanisms driving human cocaine use.

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Section: Methodsmentioning

confidence: 99%

Systems genetics of intravenous cocaine self-administration in the BXD recombinant inbred mouse panel

et al. 2015

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“…The C57BL/6J (B6) and DBA/2J (D2) mouse strains are frequently compared [19–33] because they are genetically divergent [34] and because they are the progenitor strains of the BXD recombinant inbred lines [35]. Specifically, the existence of a phenotypic difference between the progenitor strains indicates that a systems genetics approach [36] using the BXD lines could be utilized to determine the genes and gene mechanisms underlying that phenotype.…”

Section: Introductionmentioning

confidence: 99%

Performance of C57BL/6J and DBA/2J mice on a touchscreen-based attentional set-shifting task

Dickson¹,

Calton²,

Mittleman³

2014

Behavioural Brain Research

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Attentional set-shifting deficits are a feature of multiple psychiatric disorders. However, the neurogenetic mechanisms underlying these deficits are largely unknown. In the present study we assessed performance of C57BL/6J and DBA/2J mice on a touchscreen-based attentional set-shifting task similar to those used with humans and non-human primates. In experiment 1, mice discriminated simple white lines followed by compound stimuli composed of white lines superimposed on grey shapes. Although performance of the two strains was largely equivalent during early stages of the task, DBA/2J mice committed significantly more errors compared to C57BL/6J mice on the extra-dimensional shift. Additionally, performance of mice as a group declined across the three compound discrimination reversals. In experiment 2 we assessed salience of the shapes and lines dimensions and determined if dimensional salience, a variable previously shown to affect set-shifting abilities in humans and non-human primates, could be systematically manipulated. Findings from experiment 2 suggested that strain differences during the extra-dimensional shift in experiment 1 were most parsimoniously explained by a consistently impaired ability in DBA/2J mice to discriminate a subset of the compound stimuli. Additionally, unlike maze-based tasks, the relative salience of the two dimensions could be manipulated by systematically altering the width of lines exemplars while retaining other potentially-relevant attributes of the compound stimuli. These findings reveal unique and in some cases strain-dependent phenomena related to discriminations of simple and multidimensional visual stimuli which may facilitate future efforts to identify and fully characterize visual discrimination, reversal learning, and attentional set-shifting deficits in mice.

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“…In lieu of oral administration, nicotine may be subcutaneously administered via osmatic minipumps [46] , which mimics nicotine patch smoking secession treatment, or via inhalation chambers. Also, the procedures outlined herein can be extended to investigations of other drugs.…”

Section: Resultsmentioning

confidence: 99%

Multiplexed Isobaric Tag‐Based Profiling of Seven Murine Tissues Following In Vivo Nicotine Treatment Using a Minimalistic Proteomics Strategy

et al. 2018

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Nicotine is a major addictive compound in tobacco and a component of smoking-related products, such as e-cigarettes. Once internalized, nicotine can perturb many cellular pathways and can induce alterations in proteins across different cell types, however the mechanisms thereof remain undetermined. We hypothesize that both tissue-specific and global protein abundance alterations result from nicotine exposure. As such, we present the first proteome analysis of multiple tissues from nicotine-exposed mice. We treat mice via oral administration of nicotine at 200μg/mL in drinking water for 21 days. We investigate 7 tissues (brain, heart, kidney, liver, lung, pancreas, and spleen) from treated (n=5) and untreated control (n=5) mice. For each tissue, a TMT10-plex experiment (5 versus 5) was assembled. We apply a minimalistic proteomics strategy was employed using TMT reagents efficiently and fractionating by centrifugation-based reversed-phase columns to streamline sample preparation. Combined, we quantified over 11,000 non-redundant proteins from over 138,000 different peptides in 7 TMT10-plex experiments. Between 7 and 126 proteins are significantly altered in tissues from nicotine-exposed mice. Among these proteins, only 11 are altered in two or more tissues, many classified as from extracellular exosomes or involved in lipid metabolism. Our data showcase the vast extent of nicotine exposure across murine tissue.

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Genotype-dependent effects of adolescent nicotine exposure on dopamine functional dynamics in the nucleus accumbens shell in male and female mice: a potential mechanism underlying the gateway effect of nicotine

Abstract: These results suggest a genotype-dependent mechanism by which nicotine exposure during adolescence causes persistent changes in the sensitivity to "hard" stimulants such as cocaine.

Cited by 20 publications

References 85 publications

Systems genetics of intravenous cocaine self-administration in the BXD recombinant inbred mouse panel

Systems genetics of intravenous cocaine self-administration in the BXD recombinant inbred mouse panel

Performance of C57BL/6J and DBA/2J mice on a touchscreen-based attentional set-shifting task

Multiplexed Isobaric Tag‐Based Profiling of Seven Murine Tissues Following In Vivo Nicotine Treatment Using a Minimalistic Proteomics Strategy

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