ArticlePloS one2013
Changes in sensitivity of reward and motor behavior to dopaminergic, glutamatergic, and cholinergic drugs in a mouse model of fragile X syndrome.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- The striatal heterogeneous nuclear ribonucleoprotein H1 mRNA targetome associated with methamphetamine administration and behavior.Progress in neuro-psychopharmacology & biological psychiatry · 2026Article
- ErbB inhibition rescues nigral dopamine neuron hyperactivity and repetitive behaviors in a mouse model of fragile X syndrome.Molecular psychiatry · 2025Article
- Altered olfactory responses in Fmr1 KO mice.Scientific reports · 2025Article
- FMRP regulation of aggrecan mRNA translation controls perineuronal net development.Journal of neurochemistry · 2024Article
- Behavioral, neurotransmitter and transcriptomic analyses in male and femaleFrontiers in behavioral neuroscience · 2024Article
- Embryonic Valproate Exposure Alters Mesencephalic Dopaminergic Neurons Distribution and Septal Dopaminergic Gene Expression in Domestic Chicks.Frontiers in integrative neuroscience · 2022Article
- Parallel learning and cognitive flexibility impairments betweenFrontiers in behavioral neuroscience · 2022Article
- Dopaminergic Dysregulation in Syndromic Autism Spectrum Disorders: Insights From Genetic Mouse Models.Frontiers in neural circuits · 2021Review
- Altered dopaminergic pathways and therapeutic effects of intranasal dopamine in two distinct mouse models of autism.Molecular brain · 2020Article
- Protein Translation in the Nucleus Accumbens Is Dysregulated during Cocaine Withdrawal and Required for Expression of Incubation of Cocaine Craving.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Dopaminergic dysfunction in neurodevelopmental disorders: recent advances and synergistic technologies to aid basic research.Current opinion in neurobiology · 2018Review
- Decreased home cage movement and oromotor impairments in adult Fmr1-KO mice.Genes, brain, and behavior · 2017Article
- Electromyographic evidence in support of a knock-in mouse model of DYT1 Dystonia.Movement disorders : official journal of the Movement Disorder Society · 2016Article
- RNA-binding proteins, neural development and the addictions.Genes, brain, and behavior · 2016Review
- Plasma Biomarkers for Monitoring Brain Pathophysiology in FMR1 Premutation Carriers.Frontiers in molecular neuroscience · 2016Article
- Effects of the neuroactive steroid allopregnanolone on intracranial self-stimulation in C57BL/6J mice.Psychopharmacology · 2014Article
- Intracranial self-stimulation to evaluate abuse potential of drugs.Pharmacological reviews · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Fragile X syndrome (FXS) is a leading cause of intellectual disability. FXS is caused by loss of function of the FMR1 gene, and mice in which Fmr1 has been inactivated have been used extensively as a preclinical model for FXS. We investigated the behavioral pharmacology of drugs acting through dopaminergic, glutamatergic, and cholinergic systems in fragile X (Fmr1 (-/Y)) mice with intracranial self-stimulation (ICSS) and locomotor activity measurements. We also measured brain expression of tyrosine hydroxylase (TH), the rate-limiting enzyme in dopamine biosynthesis. Fmr1 (-/Y) mice were more sensitive than wild type mice to the rewarding effects of cocaine, but less sensitive to its locomotor stimulating effects. Anhedonic but not motor depressant effects of the atypical neuroleptic, aripiprazole, were reduced in Fmr1 (-/Y) mice. The mGluR5-selective antagonist, 6-methyl-2-(phenylethynyl)pyridine (MPEP), was more rewarding and the preferential M1 antagonist, trihexyphenidyl, was less rewarding in Fmr1 (-/Y) than wild type mice. Motor stimulation by MPEP was unchanged, but stimulation by trihexyphenidyl was markedly increased, in Fmr1 (-/Y) mice. Numbers of midbrain TH+ neurons in the ventral tegmental area were unchanged, but were lower in the substantia nigra of Fmr1 (-/Y) mice, although no changes in TH levels were found in their forebrain targets. The data are discussed in the context of known changes in the synaptic physiology and pharmacology of limbic motor systems in the Fmr1 (-/Y) mouse model. Preclinical findings suggest that drugs acting through multiple neurotransmitter systems may be necessary to fully address abnormal behaviors in individuals with FXS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.