Corresponding decrease in neuronal markers signals progressive parvalbumin neuron loss in MAM schizophrenia model
Open accessAbstract
Alteration in normal hippocampal (HPC) function attributed to reduced parvalbumin (PV) expression has been consistently reported in schizophrenia patients and in animal models of schizophrenia. However, it is unclear whether there is an overall loss of interneurons as opposed to a reduction in activity-dependent PV content. Co-expression of PV and the constitutively expressed substance P (SP)-receptor protein has been utilized in other models to ascertain the degree of cell survival, as opposed to reduction in activity-dependent PV content, in the HPC. The present study measured the co-expression of PV and SP-receptors in the dentate and dorsal and ventral CA3 subregions of the HPC in the methylazoymethanol acetate (MAM) rat neurodevelopmental model of schizophrenia. In addition, these changes were compared at the post-natal day 27 (PND27) and post-natal day 240 (PND > 240) time points. Brains from PND27 and PND > 240 MAM (n = 8) and saline (SAL, n = 8) treated offspring were immunohistochemically processed for the co-expression of PV and SP-receptors. The dorsal dentate, dorsal CA3 and ventral CA3 subregions of PND27 and PND > 240 MAM rats demonstrated significant reductions in PV but not SP-receptor expression, signifying a loss of PV-content. In contrast, in the ventral dentate the co-expression of PV and SP-receptors was significantly reduced only in PND > 240 MAM animals, suggesting a reduction in cell number. While MAM-induced reduction of PV content occurs in CA3 of dorsal and ventral HPC, the most substantial loss of interneuron number is localized to the ventral dentate of PND > 240 animals. The disparate loss of PV in HPC subregions likely impacts intra-HPC network activity in MAM rats.
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Some human and animal data suggest that PV-INs may remain present but cease to express PV, although a definitive conclusion cannot yet be drawn.
“Some human and animal model data suggest that formerly PV-INs are still present but cease to express PV, though a definitive conclusion cannot be drawn at this point [7,[18][19][20].”
From Parvalbumin interneuron vulnerability and brain disorders (2021) · cites this paper as [7]
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Parvalbumin interneuron vulnerability and brain disorders
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- Authors
- Gill, K. M., & Grace, A. A.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Gill, Kathryn M.
- ORCID
- Grace, Anthony A.
- Venue
- The International Journal of Neuropsychopharmacology
- Publisher
- Oxford University Press (OUP)
- Published
- 2014-04-30
- Volume
- 17
- Issue
- 10
- Pages
- 1609-1619
- ISSN
- 1461-1457 (ISSN-L)
- 1469-5111
- PMC
- PMC4161636
- OpenAlex
- W2137504997
- Cited by
- 60
- References
- 79
- Citations by year
- 2026: 7 · 2025: 2 · 2024: 3 · 2023: 3 · 2022: 7 · 2021: 5 · 2020: 5 · 2019: 3 · 2018: 7 · 2017: 3 · 2016: 8 · 2015: 7
- FWCI
- 4.58
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The International Journal of Neuropsychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (2r01mh057440-26a1)
- U.S. Public Health Service (MH57440)
- National Institute of Mental Health (MH-57440, R01-MH057440, R37MH057440)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- parvalbumin, interneuron loss, hippocampus, schizophrenia, neurokinin-1 receptor, dentate gyrus, CA3, neurodevelopmental model, neuronal markers, postnatal development
- MeSH terms
- Age Factors, Analysis of Variance, Animals, Disease Models, Animal, Gene Expression Regulation, Hippocampus, Methylazoxymethanol Acetate, Neurons, Neurotoxins, Parvalbumins, Schizophrenia, Cell Death, Receptors, Neurokinin-1, Rats
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