ArticlePharmacology, biochemistry, and behavior2013
Amphetamine-induced locomotion in a hyperdopaminergic ADHD mouse model depends on genetic background.
Article in Pharmacology, biochemistry, and behavior, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 25 citations in OpenAlex.
- Sex-dependent alterations in behavior, drug responses and dopamine transporter expression in heterozygous DAT-Cre mice.Scientific reports · 2021Article
- Altered baseline and amphetamine-mediated behavioral profiles in dopamine transporter Cre (DAT-Ires-Cre) mice compared to tyrosine hydroxylase Cre (TH-Cre) mice.Psychopharmacology · 2020Article
- Metabolic profile associated with distinct behavioral coping strategies of 129Sv and Bl6 mice in repeated motility test.Scientific reports · 2018Article
- Dopamine transporter mutant animals: a translational perspective.Journal of neurogenetics · 2016Review
- Restoration of cocaine stimulation and reward by reintroducing wild type dopamine transporter in adult knock-in mice with a cocaine-insensitive dopamine transporter.Neuropharmacology · 2014Article
- Behavior of knock-in mice with a cocaine-insensitive dopamine transporter after virogenetic restoration of cocaine sensitivity in the striatum.Neuropharmacology · 2014Article
- Food cravings, appetite, and snack-food consumption in response to a psychomotor stimulant drug: the moderating effect of "food-addiction".Frontiers in psychology · 2014Article
- Cocaine produces conditioned place aversion in mice with a cocaine-insensitive dopamine transporter.Genes, brain, and behavior · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
We previously generated a knock-in mouse line with a cocaine-insensitive dopamine transporter (DAT-CI mice). These mice lost several behavioral responses to cocaine, but retained their response to amphetamine. DAT-CI mice are hyperdopaminergic due to reduced DAT function, and may thus be a good model for studying attention deficit hyperactivity disorder (ADHD). These mice had been behaviorally characterized while they were on a mixed genetic background. However as the colony was propagated over time, the mixed genetics were shifted toward a pure C57Bl/6J background--via a common breeding scheme known as "backcrossing." Several phenotypes appeared to have changed during this time frame. In this study, we investigated whether backcrossing altered the hyperlocomotive phenotype and behavioral responses to amphetamine, a drug used to treat ADHD. C57-congenic DAT-CI mice had high spontaneous locomotor activity that could be suppressed by low doses of amphetamine. Furthermore, their locomotion was not stimulated by very high doses of amphetamine (20mg/kg). After the reversion to a mixed genetic background by breeding with the 129 strain, the C57:129 hybrid DAT-CI mice displayed reduced basal locomotor activity compared to the C57-congenic mutant mice, and regained locomotor stimulation by high-dose amphetamine. The calming effect of amphetamine at low doses was retained in both strains. In summary, reduced DAT function in DAT-CI mice leads to a hyperdopaminergic state, and an ADHD-like phenotype in both strains. The data show that the genetic background of DAT-CI mice affects their locomotor phenotypes and their responses to amphetamine. Since the differences in genetic background between the strains of mice have a significant impact on the ADHD-like phenotype and the response to amphetamine, further study with these strains could identify the genetic underpinnings affecting the severity of ADHD-related symptoms and the treatment response.
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