ArticleSchizophrenia bulletin2010
Mutant mouse models: genotype-phenotype relationships to negative symptoms in schizophrenia.
Article in Schizophrenia bulletin, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 70 citations in OpenAlex.
- Administering a Behavioral Test Battery in Rodents.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Cross species review of the physiological role of D-serine in translationally relevant behaviors.Amino acids · 2023Review
- Increased self-triggered vocalizations in an epidermal growth factor-induced rat model for schizophrenia.Scientific reports · 2022Article
- Evidence of an interaction betweenEuropean psychiatry : the journal of the Association of European Psychiatrists · 2021Article
- Behavioral Tasks Evaluating Schizophrenia-like Symptoms in Animal Models: A Recent Update.Current neuropharmacology · 2021Review
- The Effect of Chronic Methamphetamine Treatment on Schizophrenia Endophenotypes in Heterozygous Reelin Mice: Implications for Schizophrenia.Biomolecules · 2020Article
- Anxiety does not contribute to social withdrawal in the subchronic phencyclidine rat model of schizophrenia.Behavioural pharmacology · 2017Article
- Tumour necrosis factor-mediated homeostatic synaptic plasticity in behavioural models: testing a role in maternal immune activation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Article
- SorCS2 is required for BDNF-dependent plasticity in the hippocampus.Molecular psychiatry · 2016Article
- Disruption of social cognition in the sub-chronic PCP rat model of schizophrenia: Possible involvement of the endocannabinoid system.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2016Article
- Missense mutation in DISC1 C-terminal coiled-coil has GSK3β signaling and sex-dependent behavioral effects in mice.Scientific reports · 2016Article
- Parvalbumin-positive interneurons of the prefrontal cortex support working memory and cognitive flexibility.Scientific reports · 2015Article
- Toll-like receptor-2 deficiency induces schizophrenia-like behaviors in mice.Scientific reports · 2015Article
- Effects of background mutations and single nucleotide polymorphisms (SNPs) on the Disc1 L100P behavioral phenotype associated with schizophrenia in mice.Behavioral and brain functions : BBF · 2014Article
- Amotivation in schizophrenia: integrated assessment with behavioral, clinical, and imaging measures.Schizophrenia bulletin · 2014Article
- Cytokine pathway disruption in a mouse model of schizophrenia induced by Munc18-1a overexpression in the brain.Journal of neuroinflammation · 2014Article
- Neural mechanisms underlying stress resilience in Ahi1 knockout mice: relevance to neuropsychiatric disorders.Molecular psychiatry · 2014Article
- Preclinical models of antipsychotic drug action.The international journal of neuropsychopharmacology · 2013Review
- Behavioral, neurochemical and morphological changes induced by the overexpression of munc18-1a in brain of mice: relevance to schizophrenia.Translational psychiatry · 2013Article
- Advancing schizophrenia drug discovery: optimizing rodent models to bridge the translational gap.Nature reviews. Drug discovery · 2012Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Negative symptoms encompass diminution in emotional expression and motivation, some of which relate to human attributes that may not be accessible readily in animals. Additionally, their refractoriness to treatment precludes therapeutic validation of putative models. This review considers critically the application of mutant mouse models to the study of the pathobiology of negative symptoms. It focuses on 4 main approaches: genes related to the pathobiology of schizophrenia, genes associated with risk for schizophrenia, neurodevelopmental-synaptic genes, and variant approaches from other areas of neurobiology. Despite rapid advances over the past several years, it is clear that we continue to face substantive challenges in applying mutant models to better understand the pathobiology of negative symptoms: the majority of evidence relates to impairments in social behavior, with only limited data relating to anhedonia and negligible data concerning avolition and other features; even for the most widely examined feature, social behavior, studies have used diverse assessments thereof; modelling must proceed in cognizance of increasing evidence that genes and pathobiologies implicated in schizophrenia overlap with other psychotic disorders, particularly bipolar disorder. Despite the caveats and challenges, several mutant lines evidence a phenotype for at least one index of social behavior. Though this may suggest superficially some shared relationship to negative symptoms, it is not yet possible to specify either the scope or the pathobiology of that relationship for any given gene. The breadth and depth of ongoing studies in mutants hold the prospect of addressing these shortcomings.
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