ArticleFrontiers in cellular neuroscience2020
Parvalbumin-Deficiency Accelerates the Age-Dependent ROS Production in Pvalb Neurons
Article in Frontiers in cellular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Review
- Rethinking parvalbumin: From passive marker to active modulator of hippocampal circuits.IBRO neuroscience reports · 2025Article
- Single-Cell Multi-Modal Differential Analysis of the Human Neo-Cortex in HIV Infection Reveals Similarities with Hallmarks of Alzheimer's Disease.Research square · 2025Article
- Article
- Elevations in the Mitochondrial Matrix Protein Cyclophilin D Correlate With Reduced Parvalbumin Expression in the Prefrontal Cortex of Patients With Schizophrenia.Schizophrenia bulletin · 2024Article
- Antioxidant Properties Mediate Nephroprotective and Hepatoprotective Activity of Essential Oil and Hydro-Alcoholic Extract of the High-Altitude PlantAntioxidants (Basel, Switzerland) · 2023Article
- Insights into the role of intracellular calcium signaling in the neurobiology of neurodevelopmental disorders.Frontiers in neuroscience · 2023Review
- Delineating selective vulnerability of inhibitory interneurons in Alpers' syndrome.Neuropathology and applied neurobiology · 2022Article
- Article
- Developmental oxidative stress leads to T-type CaMolecular psychiatry · 2022Article
- Maternal Deprivation in Rats Decreases the Expression of Interneuron Markers in the Neocortex and Hippocampus.Frontiers in neuroanatomy · 2021Article
- The Neurometabolic Basis of Mood Instability: The Parvalbumin Interneuron Link-A Systematic Review and Meta-Analysis.Frontiers in pharmacology · 2021Review
- The Parvalbumin Hypothesis of Autism Spectrum Disorder.Frontiers in cellular neuroscience · 2020Article
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2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
In neurodevelopmental disorders (NDDs) including autism spectrum disorder (ASD) and schizophrenia, impairment/malfunctioning of a subpopulation of interneurons expressing the calcium-binding protein parvalbumin (PV) -here termed Pvalb neurons- has gradually emerged as a possible cause. These neurons may represent a hub or point-of-convergence in the etiology of NDD. Increased oxidative stress associated with mitochondria impairment in Pvalb neurons is discussed as an essential step in schizophrenia etiology. Since PV downregulation is a common finding in ASD and schizophrenia individuals and PV-deficient (PV-/-) mice show a strong ASD-like behavior phenotype, we investigated the putative link between PV expression, alterations in mitochondria and oxidative stress. In a longitudinal study with 1, 3, and 6-months old PV-/- and wild type mice, oxidative stress was investigated in 9 Pvalb neuron subpopulations in the hippocampus, striatum, somatosensory cortex, medial prefrontal cortex, thalamic reticular nucleus (TRN) and cerebellum. In Pvalb neuron somata in the striatum and TRN, we additionally determined mitochondria volume and distribution at these three time points. In all Pvalb neuron subpopulations, we observed an age-dependent increase in oxidative stress and the increase strongly correlated with PV expression levels, but not with mitochondria density in these Pvalb neurons. Moreover, oxidative stress was elevated in Pvalb neurons of PV-/- mice and the magnitude of the effect was again correlated with PV expression levels in the corresponding wild type Pvalb neuron subpopulations. The PV-dependent effect was insignificant at 1 month and relative differences between WT and PV-/- Pvalb neurons were largest at 3 months. Besides the increase in mitochondria volume in PV's absence in TRN and striatal PV-/- Pvalb neurons fully present already at 1 month, we observed a redistribution of mitochondria from the perinuclear region toward the plasma membrane at all time points. We suggest that in absence of PV, slow Ca
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