Animal models of schizophrenia
Open accessAbstract
Developing reliable, predictive animal models for complex psychiatric disorders, such as schizophrenia, is essential to increase our understanding of the neurobiological basis of the disorder and for the development of novel drugs with improved therapeutic efficacy. All available animal models of schizophrenia fit into four different induction categories: developmental, drug‐induced, lesion or genetic manipulation, and the best characterized examples of each type are reviewed herein. Most rodent models have behavioural phenotype changes that resemble ‘positive‐like’ symptoms of schizophrenia, probably reflecting altered mesolimbic dopamine function, but fewer models also show altered social interaction, and learning and memory impairment, analogous to negative and cognitive symptoms of schizophrenia respectively. The negative and cognitive impairments in schizophrenia are resistant to treatment with current antipsychotics, even after remission of the psychosis, which limits their therapeutic efficacy. The MATRICS initiative developed a consensus on the core cognitive deficits of schizophrenic patients, and recommended a standardized test battery to evaluate them. More recently, work has begun to identify specific rodent behavioural tasks with translational relevance to specific cognitive domains affected in schizophrenia, and where available this review focuses on reporting the effect of current and potential antipsychotics on these tasks. The review also highlights the need to develop more comprehensive animal models that more adequately replicate deficits in negative and cognitive symptoms. Increasing information on the neurochemical and structural CNS changes accompanying each model will also help assess treatments that prevent the development of schizophrenia rather than treating the symptoms, another pivotal change required to enable new more effective therapeutic strategies to be developed. LINKED ARTICLES This article is part of a themed issue on Translational Neuropharmacology. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2011.164.issue‐4
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Non-competitive NMDA receptor antagonists such as ketamine or PCP have been increasingly used in animal models of schizophrenia and induce hyperlocomotion, social withdrawal, and impairment of cognition and pre-pulse inhibition in rodents.
“Thus, non-competitive agonists that blockade the NMDA receptor, such as ketamine or phencyclidine (PCP), have been increasingly used in animal models of schizophrenia and have been shown to induce hyperlocomotion, social withdrawal, and impairment of both cognition and pre-pulse inhibition in rodents [100].”
From Prenatal nicotine exposure during pregnancy results in adverse neurodevelopmental alterations and neurobehavioral deficits (2023) · cites this paper as [100]
The “PCP models of schizophrenia” section (page unavailable) identifies ketamine and PCP as non-competitive NMDA receptor antagonists and reports reduced social interaction, cognitive impairment, and impaired prepulse inhibition in rodents after PCP or NMDA-antagonist administration. But the claim omits important regimen-dependent qualifications: chronic PCP does not cause spontaneous hyperactivity, instead sensitizing locomotion to a later PCP dose, and its prepulse-inhibition deficit diminishes after cessation. The cited passages also do not establish that use of these models has increased. (LLM, conf=0.85)
Experimental — accuracy not yet measuredNeurodevelopmental models of schizophrenia in animals typically involve exposure of the neonate during gestation or the perinatal period to adverse environmental insults such as maternal stress, hypoxia, malnutrition, or post-weaning social isolation that alter brain development and cause behavioral deficits into adulthood.
“Neurodevelopmental models of schizophrenia in animals typically involve exposure of the neonate, either during gestation or the perinatal period, to adverse environmental insults such as maternal stress, hypoxia, malnutrition, or post-weaning social isolation that alter the brain development and cause behavioral deficits into adulthood [100–102].”
From Prenatal nicotine exposure during pregnancy results in adverse neurodevelopmental alterations and neurobehavioral deficits (2023) · cites this paper as [100]
Animal models of schizophrenia typically fit into four induction categories including drug-induced, lesion or genetic manipulation, and developmental studies.
“Animal models of schizophrenia typically fit into four different induction categories including drug-induced, lesion or genetic manipulation, and developmental studies [100].”
From Prenatal nicotine exposure during pregnancy results in adverse neurodevelopmental alterations and neurobehavioral deficits (2023) · cites this paper as [100]
Mice carrying mutations in a handful of genes reproduce neuroanatomical, functional and behavioral deficits observed in schizophrenia.
“In addition, mice carrying mutations in a handful of genes reproduce neuroanatomical, functional and behavioral deficits observed in schizophrenia 57 ,”
From Developmental timing and critical windows for the treatment of psychiatric disorders (2016) · cites this paper as [57]
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- Authors
- Jones, C., Watson, D., & Fone, K.
- Affiliations
- University of Nottingham (GB)
- Venue
- British Journal of Pharmacology
- Publisher
- Wiley
- Published
- 2011-10
- Volume
- 164
- Issue
- 4
- Pages
- 1162-1194
- ISSN
- 0007-1188 (ISSN-L)
- 1476-5381
- PMC
- PMC3229756
- OpenAlex
- W1490681631
- Cited by
- 771
- References
- 26
- Citations by year
- 2026: 32 · 2025: 30 · 2024: 48 · 2023: 49 · 2022: 68 · 2021: 83 · 2020: 74 · 2019: 65 · 2018: 55 · 2017: 60 · 2016: 44 · 2015: 59 · 2014: 45 · 2013: 29 · 2012: 18
- FWCI
- 4.28
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- British Journal of Pharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Eli Lilly and Company
- GlaxoSmithKline
- F. Hoffmann-La Roche
- Servier
- Medical Research Council
- Biotechnology and Biological Sciences Research Council
- Institut de Recherches Servier
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- schizophrenia, animal models, rodent models, positive symptoms, negative symptoms, cognitive impairment, mesolimbic dopamine system, antipsychotic efficacy, cognitive tasks, developmental model, genetic engineering, lesion models, social interaction, learning and memory impairment, MATRICS
- MeSH terms
- Amphetamine, Animals, Cognition Disorders, Disease Models, Animal, Female, Humans, Male, Models, Genetic, Models, Neurological, Neuropsychological Tests, Schizophrenia, Antipsychotic Agents, Mice, Rats
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