Atypical antipsychotics clozapine and quetiapine attenuate prepulse inhibition deficits in dopamine transporter knockout mice
Open accessAbstract
Sensorimotor gating disruptions are seen in various psychiatric illnesses with putatively different pathologies, including schizophrenia and bipolar disorder. Interestingly, mice lacking the dopamine (DA) transporter (DAT) gene display markedly increased levels of DA, deficits in sensorimotor gating, and hyperactivity relative to wild-type mice. Atypical antipsychotics are effective treatments of schizophrenia and manic symptoms, presumably in part by antagonizing DA receptors. Here we report that treatment with clozapine (3 mg/kg) or quetiapine (2.5 mg/kg) attenuated prepulse inhibition deficits in male DAT knockout mice. Thus male DAT knockout mice may provide a useful animal model for predicting the efficacy of novel drugs in treating psychiatric illnesses characterized by a dysregulated DA system.
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DAT knockout mice phenotypes resemble amphetamine-like effects, and both hyperlocomotion and PPI deficits can be reversed with D1 or D2 receptor antagonists, atypical antipsychotics clozapine and quetiapine, various antidepressant drugs, and monoamine transporter inhibitors.
“The DAT knockout mice phenotypes resemble amphetamine-like effects, and both hyperlocomotion and PPI deficits can be reversed with either D1 or D2 receptor antagonists [376], the atypical antipsychotics clozapine and quetiapine [377], various antidepressant drugs, and monoamine transporter inhibitors [378].”
From Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings (2012) · cites this paper as [377]
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References 27 · Cited by 57
- Authors
- Powell, S. B., Young, J. W., Ong, J. C., Caron, M. G., & Geyer, M. A.
- Affiliations
- University of California San Diego (US)
- Duke University (US)
- Corresponding author
- Powell, Susan B.
- Venue
- Behavioural Pharmacology
- Published
- 2008-09
- Volume
- 19
- Issue
- 5-6
- Pages
- 562-565
- ISSN
- 0955-8810 (ISSN-L)
- PMC
- PMC2693185
- OpenAlex
- W2009033786
- Cited by
- 57
- References
- 27
- Citations by year
- 2025: 1 · 2023: 1 · 2022: 3 · 2021: 1 · 2020: 1 · 2019: 2 · 2017: 6 · 2016: 1 · 2015: 5 · 2014: 5 · 2013: 6 · 2012: 8
- FWCI
- 3.75
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Behavioural Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (MH60451, MH42228, R37MH042228, R01MH071916, R01MH042228, P50MH060451, MH071916)
- National Institute of Neurological Disorders and Stroke (NS-19576, R01NS019576)
- 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 › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- clozapine, quetiapine, atypical antipsychotics, prepulse inhibition, sensorimotor gating, dopamine transporter knockout mice, dopamine dysregulation, schizophrenia, bipolar disorder, hyperactivity
- MeSH terms
- Quetiapine Fumarate, Animals, Clozapine, Dibenzothiazepines, Disease Models, Animal, Injections, Intraperitoneal, Mice, Mutant Strains, Schizophrenia, Reflex, Startle, Antipsychotic Agents, Mice, Knockout, Dopamine Plasma Membrane Transport Proteins, Mice
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