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The Dopamine D2, but not D3or D4, Receptor Subtype is Essential for the Disruption of Prepulse Inhibition Produced by Amphetamine in Mice
Open accessAbstract
Brain dopamine (DA) systems are involved in the modulation of the sensorimotor gating phenomenon known as prepulse inhibition (PPI). The class of D2-like receptors, including the D2, D3, and D4 receptor subtypes, have all been implicated in the control of PPI via studies of DA agonists and antagonists in rats. Nevertheless, the functional relevance of each receptor subtype remains unclear because these ligands are not specific. To determine the relevance of each receptor subtype, we used genetically altered strains of “knock-out” mice lacking the DA D2, D3, or D4 receptors. We tested the effects of each knock-out on both the phenotypic expression of PPI and the disruption of PPI produced by the indirect DA agonist d-amphetamine (AMPH). No phenotypic differences in PPI were observed at baseline. AMPH significantly disrupted PPI in the D2 (+/+) mice but had no effect in the D2 (−/−) mice. After AMPH treatment, both DA D3 and D4 receptor (+/+) and (−/−) mice had significant disruptions in PPI. These findings indicate that the AMPH-induced disruption of PPI is mediated via the DA D2 receptor and not the D3 or D4 receptor subtypes. Uncovering the neural mechanisms involved in PPI will further our understanding of the substrates of sensorimotor gating and could lead to better therapeutics to treat gating disorders, such as schizophrenia.
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“Studies in mice have indicated that administration of direct-acting DA agonists (such as apomorphine) and indirect DA agonists (such as cocaine) to mice disrupt PPI primarily via D1 receptors [369], whereas D2 receptors seem to modulate amphetamine-induced PPI deficits [370].”
From Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings (2012) · cites this paper as [370]
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Metadata
- Authors
- Ralph, R. J., Varty, G. B., Kelly, M. A., Wang, Y.-M., Caron, M. G., Rubinstein, M., Grandy, D. K., Low, M. J., & Geyer, M. A.
- Affiliations
- University of California San Diego (US)
- Vollum Institute (US)
- Howard Hughes Medical Institute (US)
- Consejo Nacional de Investigaciones Científicas y Técnicas (AR)
- Oregon Health & Science University (US)
- ORCID
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1999-06-01
- Volume
- 19
- Issue
- 11
- Pages
- 4627-4633
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6782596
- OpenAlex
- W2100216270
- Cited by
- 174
- References
- 38
- Citations by year
- 2026: 1 · 2024: 2 · 2023: 2 · 2022: 2 · 2021: 1 · 2019: 3 · 2018: 4 · 2017: 1 · 2016: 3 · 2015: 2 · 2014: 5 · 2013: 5 · 2012: 6
- FWCI
- 5.38
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- National Alliance for Research on Schizophrenia and Depression
- National Institute of Mental Health (K05-MH01228, F31MH012086)
- National Institute on Drug Abuse
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- prepulse inhibition, sensorimotor gating, dopamine D2 receptor, dopamine D3 receptor, dopamine D4 receptor, amphetamine, receptor knockout mice, schizophrenia
- MeSH terms
- Acoustic Stimulation, Amphetamine, Animals, Mice, Mutant Strains, Neural Inhibition, Receptors, Dopamine, Reflex, Startle, Dopamine Agents, Receptors, Dopamine D2, Mice, Knockout, Receptors, Dopamine D3, Receptors, Dopamine D4, Mice
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