ArticleMolecular neurobiology2016
Environmental Enrichment Prevent the Juvenile Hypoxia-Induced Developmental Loss of Parvalbumin-Immunoreactive Cells in the Prefrontal Cortex and Neurobehavioral Alterations Through Inhibition of NADPH Oxidase-2-Derived Oxidative Stress.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.
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Who cites it
12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 14 citations in OpenAlex.
- The impact of enriched environments on cerebral oxidative balance in rodents: a systematic review of environmental variability effects.Frontiers in neuroscience · 2024Pooled it
- Effect of environmental enrichment on behavioral and morphological outcomes following neonatal hypoxia-ischemia in rodent models: A systematic review and meta-analysis.Molecular neurobiology · 2022Pooled it
- Vitamin C mitigates early auditory cortical hyperexcitability and antioxidant imbalance induced by acute intermittent hypoxia.Experimental brain research · 2026Article
- The role of sensory experience in the maturation of prefrontal cortical circuits.Frontiers in neuroscience · 2026Review
- Short-term environmental enrichment modulates brain region-specific redox responses in adolescent female mice.Frontiers in aging neuroscience · 2026Article
- Sleep-dependent alterations in anterior cingulate cortex excitation-inhibition balance link alterations in BOLD-CSF coupling to cognitive performance in obstructive sleep apnea.Frontiers in aging neuroscience · 2026Article
- Introducing the brain erythropoietin circle to explain adaptive brain hardware upgrade and improved performance.Molecular psychiatry · 2022Review
- Antioxidant and antiradical activities depend on adrenal tumor type.Frontiers in endocrinology · 2022Article
- Timely N-Acetyl-Cysteine and Environmental Enrichment Rescue Oxidative Stress-Induced Parvalbumin Interneuron Impairments via MMP9/RAGE Pathway: A Translational Approach for Early Intervention in Psychosis.Schizophrenia bulletin · 2021Article
- Antioxidant Barrier and Oxidative Damage to Proteins, Lipids, and DNA/RNA in Adrenal Tumor Patients.Oxidative medicine and cellular longevity · 2021Article
- HIF-1α-Mediated, NADPH Oxidase-Derived ROS Contributes to Laryngeal Airway Hyperreactivity Induced by Intermittent Hypoxia in Rats.Frontiers in physiology · 2020Article
- Effect of Hypoxic Injury in Mood Disorder.Neural plasticity · 2017Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We compared the expression of phenotype of parvalbumin (PV)-immunoreactive cells in the prefrontal cortex (PFC) of juvenile rats reared in enriched environment (EE) after daily intermittent hypoxia (IH) exposure to those reared in standard environment (SE) and investigated the involvement of NADPH oxidase-2 (NOX2)-derived oxidative stress in the IH-induced neurodevelopmental and neurobehavioral consequences in a juvenile rat model of obstructive sleep apnea. Postnatal day 21 (P21) rats were exposed to IH or room air 8 h daily for 14 consecutive days. After the daily exposure, the rats were raised in SE or EE. In the PFC of P34 rats, we determined the impact (i) of IH exposures on NOX2-derived oxidative stress and PV immunoreactivity, (ii) of pharmacological NOX2 inhibition on IH-induced oxidative stress and PV immunoreactivity, and (iii) of EE on the IH-induced oxidative stress and PV immunoreactivity. Behavioral testing of psychiatric anxiety was carried out consecutively in the open-field test and elevated plus maze at P35 and P36. The results showed IH exposures increased NOX2 expression in the PFC of P34 rats, which was accompanied with elevation of NOX activity and indirect markers of oxidative stress (4-HNE). IH exposures increased 4-HNE immunoreactivity in cortical PV cells, which was accompanied with reduction of PV immunoreactivity. Treatment of IH rats with the antioxidant/NOX inhibitor apocynin prevented the PV cells loss in the PFC and reversed the IH-induced psychiatric anxiety. EE attenuated the NOX2-derived oxidative stress and reversed the PV-immunoreactivity reduction in the PFC induced by IH. Our data suggest that EE might prevent the juvenile hypoxia-induced developmental loss of PV cells in the PFC and attenuate the neurobehavioral alterations through inhibition of NOX2-derived oxidative stress.
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