The DOI matches its Crossref record; 110 of the 110 references it cites were found in a registry or an index.
Postnatal Phencyclidine Administration Selectively Reduces Adult Cortical Parvalbumin-Containing Interneurons
Abstract
Transient postnatal NMDA receptor blockade by phencyclidine (PCP), ketamine, or MK-801 induces developmental neuroapoptosis and adult behavioral deficits, which resemble abnormal human behaviors typically present in schizophrenia. This study tested the hypothesis that PCP-induced developmental apoptosis causes a specific deficit of GABAergic interneurons containing parvalbumin (PV), calretinin (CR), or calbindin (CB). Young adult (PND56) rats that were given a single dose of PCP (10 mg/kg) on PND7 exhibited no densitometric change of either CR or CB neurons in any brain region studied, but demonstrated a selective deficit of PV-containing neurons in the superficial layers (II-IV) of the primary somatosensory (S1), motor (M), and retrosplenial cortices, but not in the striatum (CPu) or hippocampus. Further, CR and CB neurons, which were expressed at the time of PCP administration, showed no colocalization with cellular markers of apoptosis (terminal dUTP nick-end labeling (TUNEL) of broken DNA or cleaved caspase-3), indicating that CR- and CB-containing neurons were protected from the toxic effect of PCP and survived into adulthood. This suggests that the deletion of PV neurons occurred during development, but cleaved caspase-3 showed no colocalization with BrdU, a specific marker of S-phase proliferation. These data suggest that the loss of PV-containing neurons was not due to an effect of PCP on proliferating neurons, but rather an effect on post-mitotic neurons. The developmental dependence and neuronal specificity of this effect of PCP provides further evidence that this model may be valuable in exploring the pathophysiology of schizophrenia.
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In the citing paper
“However, PVI are especially vulnerable to NMDAR hypofunction during development (Abekawa et al., 2007; Powell et al., 2012; Wang et al., 2008; Wang et al., 2013).”
From Redox dysregulation, neuroinflammation, and NMDA receptor hypofunction: A “central hub” in schizophrenia pathophysiology? (2016) · cites this paper as Wang et al., 2008
In the citing paper
“early postnatal PCP reduces the number of adult PVþ neurons in the PFC.58”
From Adolescent Onset of Cortical Disinhibition in Schizophrenia: Insights From Animal Models (2011) · cites this paper as [58]
Citations
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Cited by
Sorted by citations
Ketamine-Induced Loss of Phenotype of Fast-Spiking Interneurons Is Mediated by NADPH-Oxidase
Behrens, M. M., Ali, S. S., Dao, D. N., Lucero, J., Shekhtman, G., Quick, K. L., & Dugan, L. L. (2007) · Science · doi:10.1126/science.1148045 · Cited by 585
Neill, J. C., Barnes, S. A., Cook, S., Grayson, B., Idris, N. F., McLean, S. L., Snigdha, S., Rajagopal, L., & Harte, M. (2010) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2010.07.004 · Cited by 541
GABAergic interneuron origin of schizophrenia pathophysiology
Nakazawa, K., Zsiros, V., Jiang, Z., Nakao, K., Kolata, S., Zhang, S., & Belforte, J. E. (2012) · Neuropharmacology · doi:10.1016/j.neuropharm.2011.01.022 · Cited by 498
Kantrowitz, J. T., & Javitt, D. C. (2010) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2010.04.006 · Cited by 414
Steullet, P., Cabungcal, J.-H., Coyle, J., Didriksen, M., Gill, K., Grace, A. A., Hensch, T. K., LaMantia, A.-S., Lindemann, L., Maynard, T. M., et al. (2017) · Molecular Psychiatry · doi:10.1038/mp.2017.47 · Cited by 360
Metadata
- Authors
- Wang, C. Z., Yang, S. F., Xia, Y., & Johnson, K. M.
- Affiliations
- The University of Texas Medical Branch at Galveston (US)
- Corresponding author
- Wang, Cheng Z
- Johnson, Kenneth M
- ORCID
- Xia, Yan
- Venue
- Neuropsychopharmacology
- Published
- 2007-12-05
- Volume
- 33
- Issue
- 10
- Pages
- 2442-2455
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- OpenAlex
- W2026782090
- Cited by
- 161
- References
- 110
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 1 · 2023: 2 · 2022: 1 · 2021: 3 · 2020: 4 · 2019: 9 · 2018: 6 · 2017: 9 · 2016: 6 · 2015: 13 · 2014: 13 · 2013: 11 · 2012: 7
- FWCI
- 5.48
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neuropsychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Health and Human Services
- University of Texas Medical Branch
- National Institutes of Health (5r01mh063871-04)
- National Institute of Mental Health (MH63871)
- National Institute on Drug Abuse (DA 02073, R01DA002073)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Anesthesia and Neurotoxicity Research
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- phencyclidine, NMDA receptor blockade, parvalbumin interneurons, calretinin, calbindin, GABAergic interneurons, schizophrenia model, postnatal drug exposure, caspase-3, TUNEL, somatosensory cortex, motor cortex, retrosplenial cortex
- MeSH terms
- Animals, Animals, Newborn, Bromodeoxyuridine, Cell Count, Cell Survival, Cerebral Cortex, Disease Models, Animal, Female, Interneurons, Male, Parvalbumins, Phencyclidine, Schizophrenia, Time, Rats, Sprague-Dawley, Apoptosis, Excitatory Amino Acid Antagonists, Cell Proliferation, Rats, Caspase 3, Calbindins, S100 Calcium Binding Protein G, Calbindin 2
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