ArticleFrontiers in cellular neuroscience2017
p47Phox/CDK5/DRP1-Mediated Mitochondrial Fission Evokes PV Cell Degeneration in the Rat Dentate Gyrus Following Status Epilepticus.
Article in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 32 citations in OpenAlex.
- Mitochondrial fission inhibitor Mdivi-1 alleviates lipopolysaccharide-induced parvalbumin interneurons dysregulation and cognitive impairments in a mouse model of sepsis-associated encephalopathy.Frontiers in pharmacology · 2025Article
- Reciprocal regulation of oxidative stress and mitochondrial fission augments parvalbumin downregulation through CDK5-DRP1- and GPx1-NF-κB signaling pathways.Cell death & disease · 2024Article
- Disrupted brain mitochondrial morphology after in vivo hydrogen sulfide exposure.Scientific reports · 2023Article
- EGCG Attenuates CA1 Neuronal Death by Regulating GPx1, NF-κB S536 Phosphorylation and Mitochondrial Dynamics in the Rat Hippocampus following Status Epilepticus.Antioxidants (Basel, Switzerland) · 2023Article
- CDDO-Me Attenuates CA1 Neuronal Death by Facilitating RalBP1-Mediated Mitochondrial Fission and 4-HNE Efflux in the Rat Hippocampus Following Status Epilepticus.Antioxidants (Basel, Switzerland) · 2022Article
- Glutathione Regulates GPx1 Expression during CA1 Neuronal Death and Clasmatodendrosis in the Rat Hippocampus following Status Epilepticus.Antioxidants (Basel, Switzerland) · 2022Article
- Transcranial photobiomodulation add-on therapy to valproic acid for pentylenetetrazole-induced seizures in peripubertal rats.BMC complementary medicine and therapies · 2022Article
- The role of Cdk5 in neurological disorders.Frontiers in cellular neuroscience · 2022Review
- Transcranial photobiomodulation (808 nm) attenuates pentylenetetrazole-induced seizures by suppressing hippocampal neuroinflammation, astrogliosis, and microgliosis in peripubertal rats.Neurophotonics · 2022Article
- Mechanisms of disease-modifying effect of saracatinib (AZD0530), a Src/Fyn tyrosine kinase inhibitor, in the rat kainate model of temporal lobe epilepsy.Neurobiology of disease · 2021Article
- Mdivi-1 alleviates brain damage and synaptic dysfunction after intracerebral hemorrhage in mice.Experimental brain research · 2021Article
- LONP1 Regulates Mitochondrial Accumulations of HMGB1 and Caspase-3 in CA1 and PV Neurons Following Status Epilepticus.International journal of molecular sciences · 2021Article
- The Neurometabolic Basis of Mood Instability: The Parvalbumin Interneuron Link-A Systematic Review and Meta-Analysis.Frontiers in pharmacology · 2021Review
- Nuclear Factor-Erythroid 2-Related Factor 2 (Nrf2) and Mitochondrial Dynamics/Mitophagy in Neurological Diseases.Antioxidants (Basel, Switzerland) · 2020Review
- A Composite Sketch of Fast-Spiking Parvalbumin-Positive Neurons.Cerebral cortex communications · 2020Article
- The Regional Specific Alterations in BBB Permeability are Relevant to the Differential Responses of 67-kDa LR Expression in Endothelial Cells and Astrocytes Following Status Epilepticus.International journal of molecular sciences · 2019Article
- Mitochondrial dynamics and their potential as a therapeutic target.Mitochondrion · 2019Review
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- Blockade of AMPA Receptor Regulates Mitochondrial Dynamics by Modulating ERK1/2 and PP1/PP2A-Mediated DRP1-S616 Phosphorylations in the Normal Rat Hippocampus.Frontiers in cellular neuroscience · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parvalbumin (PV) is one of the calcium-binding proteins, which plays an important role in the responsiveness of inhibitory neurons to an adaptation to repetitive spikes. Furthermore, PV neurons are highly vulnerable to status epilepticus (SE, prolonged seizure activity), although the underlining mechanism remains to be clarified. In the present study, we found that p47Phox expression was transiently and selectively increased in PV neurons 6 h after SE. This up-regulated p47Phox expression was accompanied by excessive mitochondrial fission. In this time point, CDK5-tyrosine 15 and dynamin-related protein 1 (DRP1)-serine 616 phosphorylations were also increased in PV cells. Apocynin (a p47Phox inhibitor) effectively mitigated PV cell loss via inhibition of CDK5/DRP1 phosphorylations and mitochondrial fragmentation induced by SE. Roscovitine (a CDK5 inhibitor) and Mdivi-1 (a DRP1 inhibitor) attenuated SE-induced PV cell loss by inhibiting aberrant mitochondrial fission. These findings suggest that p47Phox/CDK5/DRP1 may be one of the important upstream signaling pathways in PV cell degeneration induced by SE via excessive mitochondrial fragmentation.
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