ArticleTranslational psychiatry2017
A mouse model of the schizophrenia-associated 1q21.1 microdeletion syndrome exhibits altered mesolimbic dopamine transmission.
Article in Translational psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 53 citations in OpenAlex.
- Developmentally dynamic, non-convergent transcriptomic profiles in CNV models for schizophrenia risk.Molecular psychiatry · 2026Article
- Human induced pluripotent stem cell-derived microglia with 1q21.1 deletion and duplication exhibit aberrant inflammatory response.Genes & diseases · 2026Article
- How copy number variations shape brain developmental disorders: Unraveling the synaptic puzzle.Psychiatry and clinical neurosciences · 2026Review
- HIF-1 Targeting Intervention Renders Protection From Alzheimer's-Like Pathology in a Humanized Mice Model of HIV Infection.Journal of extracellular vesicles · 2025Article
- Disrupted transcriptional networks regulated by CHD1L during neurodevelopment underlie the mirrored neuroanatomical and growth phenotypes of the 1q21.1 copy number variant.Nucleic acids research · 2025Article
- An ace in the hole? Opportunities and limits of using mice to understand schizophrenia neurobiology.Molecular psychiatry · 2025Review
- Rare Copy Number Variants Reveal Critical Cell Types and Periods of Brain Development in Neurodevelopmental Disorders.Biological psychiatry global open science · 2025Article
- A review on the relationship between the distal 1q21.1 microdeletion and schizophrenia.Frontiers in genetics · 2025Review
- Brain metabolic profiling of schizophrenia: a path towards a better understanding of the neuropathogenesis of psychosis.Metabolic brain disease · 2024Review
- A genetic-epigenetic interplay at 1q21.1 locus underlies CHD1L-mediated vulnerability to primary progressive multiple sclerosis.Nature communications · 2024Article
- Mechanisms of copy number variants in neuropsychiatric disorders: From genes to therapeutics.Current opinion in neurobiology · 2023Review
- Copy Number Variations in Neuropsychiatric Disorders.International journal of molecular sciences · 2023Review
- The contribution of copy number variants to psychiatric symptoms and cognitive ability.Molecular psychiatry · 2023Review
- Current advancements of modelling schizophrenia using patient-derived induced pluripotent stem cells.Acta neuropathologica communications · 2022Review
- Behavioural and molecular characterisation of the Dlg2 haploinsufficiency rat model of genetic risk for psychiatric disorder.Genes, brain, and behavior · 2022Article
- Dopamine transporter silencing in the rat: systems-level alterations in striato-cerebellar and prefrontal-midbrain circuits.Molecular psychiatry · 2022Article
- Using induced pluripotent stem cells to investigate human neuronal phenotypes in 1q21.1 deletion and duplication syndrome.Molecular psychiatry · 2022Article
- Effects of copy number variations on brain structure and risk for psychiatric illness: Large-scale studies from the ENIGMA working groups on CNVs.Human brain mapping · 2022Review
- Computational identification of variables in neonatal vocalizations predictive for postpubertal social behaviors in a mouse model of 16p11.2 deletion.Molecular psychiatry · 2021Article
- Haloperidol rescues the schizophrenia-like phenotype in adulthood after rotenone administration in neonatal rats.Psychopharmacology · 2021Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1q21.1 hemizygous microdeletion is a copy number variant leading to eightfold increased risk of schizophrenia. In order to investigate biological alterations induced by this microdeletion, we generated a novel mouse model (Df(h1q21)/+) and characterized it in a broad test battery focusing on schizophrenia-related assays. Df(h1q21)/+ mice displayed increased hyperactivity in response to amphetamine challenge and increased sensitivity to the disruptive effects of amphetamine and phencyclidine hydrochloride (PCP) on prepulse inhibition. Probing of the direct dopamine (DA) pathway using the DA D1 receptor agonist SKF-81297 revealed no differences in induced locomotor activity compared to wild-type mice, but Df(h1q21)/+ mice showed increased sensitivity to the DA D2 receptor agonist quinpirole and the D1/D2 agonist apomorphine. Electrophysiological characterization of DA neuron firing in the ventral tegmental area revealed more spontaneously active DA neurons and increased firing variability in Df(h1q21)/+ mice, and decreased feedback reduction of DA neuron firing in response to amphetamine. In a range of other assays, Df(h1q21)/+ mice showed no difference from wild-type mice: gross brain morphology and basic functions such as reflexes, ASR, thermal pain sensitivity, and motor performance were unaltered. Similarly, anxiety related measures, baseline prepulse inhibition, and seizure threshold were unaltered. In addition to the central nervous system-related phenotypes, Df(h1q21)/+ mice exhibited reduced head-to tail length, which is reminiscent of the short stature reported in humans with 1q21.1 deletion. With aspects of both construct and face validity, the Df(h1q21)/+ model may be used to gain insight into schizophrenia-relevant alterations in dopaminergic transmission.
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