Glutathione deficit during development induces anomalies in the rat anterior cingulate GABAergic neurons: Relevance to schizophrenia
Open accessAbstract
A series of studies in schizophrenic patients report a decrease of glutathione (GSH) in prefrontal cortex (PFC) and cerebrospinal fluid, a decrease in mRNA levels for two GSH synthesizing enzymes and a deficit in parvalbumin (PV) expression in a subclass of GABA neurons in PFC. GSH is an important redox regulator, and its deficit could be responsible for cortical anomalies, particularly in regions rich in dopamine innervation. We tested in an animal model if redox imbalance (GSH deficit and excess extracellular dopamine) during postnatal development would affect PV-expressing neurons. Three populations of interneurons immunolabeled for calcium-binding proteins were analyzed quantitatively in 16-day-old rat brain sections. Treated rats showed specific reduction in parvalbumin immunoreactivity in the anterior cingulate cortex, but not for calbindin and calretinin. These results provide experimental evidence for the critical role of redox regulation in cortical development and validate this animal model used in schizophrenia research.
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A pharmacologically induced transient postnatal glutathione deficit causes both immediate and long-term decreased density of parvalbumin-immunoreactive cells in the anterior cingulate cortex.
“A pharmacologically induced transient postnatal deficit in GSH causes both immediate and long-term decreased density of parvalbumin-immunoreactive cells in the anterior cingulate cortex (ACC) (Cabungcal et al., 2006; Kulak et al., 2013; Steullet et al., 2011).”
From Redox dysregulation, neuroinflammation, and NMDA receptor hypofunction: A “central hub” in schizophrenia pathophysiology? (2016) · cites this paper as Cabungcal et al., 2006
In rodent models of brain disorders, higher oxidative stress consistently correlates with fewer PV-positive cortical interneurons.
“In rodent models that recapitulate aspects of brain disorders, higher oxidative stress consistently correlates with decreased PV-positive cortical interneurons [92,93].”
From Parvalbumin interneuron vulnerability and brain disorders (2021) · cites this paper as [93]
PVIs are vulnerable to redox dysregulation/oxidative stress.
“Indeed, PVIs are vulnerable to redox dysregulation/oxidative stress.37, 38, 39, 40”
From Oxidative stress-driven parvalbumin interneuron impairment as a common mechanism in models of schizophrenia (2017) · cites this paper as [38]
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References 105 · Cited by 96
- Authors
- Cabungcal, J.-H., Nicolas, D., Kraftsik, R., Cuénod, M., Do, K. Q., & Hornung, J.-P.
- Affiliations
- Centre Hospitalier Universitaire Vaudois (CH)
- University of Lausanne (CH)
- Corresponding author
- Cabungcal, Jan-Harry
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2006-06
- Volume
- 22
- Issue
- 3
- Pages
- 624-637
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W2004497754
- Cited by
- 96
- References
- 105
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 2 · 2023: 4 · 2022: 2 · 2021: 6 · 2020: 3 · 2019: 2 · 2018: 2 · 2017: 3 · 2016: 3 · 2015: 5 · 2014: 11 · 2013: 6 · 2012: 7
- FWCI
- 2.97
- Type
- journal article
- Language
- en
- Open access
- green
- doaj.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- IRIS (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion)
- 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 › Biochemistry, Genetics and Molecular Biology › Biochemistry › Sulfur Compounds in Biology
- Keywords
- redox imbalance, parvalbumin, GABAergic interneurons, anterior cingulate cortex, schizophrenia, postnatal brain development, prefrontal cortex, glutathione synthetase, calcium-binding proteins, animal models of schizophrenia
- MeSH terms
- Animals, Brain Chemistry, Disease Models, Animal, Dopamine, gamma-Aminobutyric Acid, Glutathione, Immunohistochemistry, Male, Neurons, Parvalbumins, Schizophrenia, Prefrontal Cortex, Extracellular Fluid, Rats, Calbindins, S100 Calcium Binding Protein G, Calbindin 2
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