ArticleScientific reports2016
Spatiotemporal profile of Map2 and microglial changes in the hippocampal CA1 region following pilocarpine-induced status epilepticus.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- Temporal profiling of hippocampal astrocyte reactivity reveals persistent GFAP cleavage and complement C3 association after status epilepticus.Brain structure & function · 2026Article
- Severity-dependent proteomic alterations in the rat hippocampus following pilocarpine-induced status epilepticus.Molecular and cellular neurosciences · 2026Article
- Severity-dependent proteomic alterations in the rat hippocampus following pilocarpine-induced status epilepticus.bioRxiv : the preprint server for biology · 2026Article
- Context-tuned strategies for marker selection precision in neuronal studies.Frontiers in neuroscience · 2026Review
- Cytoprotective and Immunomodulatory Properties of Mesenchymal Stem Cell Secretome and Its Effect on Organotypic Hippocampal Cultures in Mouse Model of Temporal Lobe Epilepsy.International journal of molecular sciences · 2025Article
- Review
- Acute depletion of complement C3 with cobra venom factor attenuates memory deficits induced by status epilepticus.Epilepsia open · 2024Article
- Effects of L-Type Voltage-Gated Calcium Channel (LTCC) Inhibition on Hippocampal Neuronal Death after Pilocarpine-Induced Seizure.Antioxidants (Basel, Switzerland) · 2024Article
- Evaluation of Midazolam-Ketamine-Allopregnanolone Combination Therapy against Cholinergic-Induced Status Epilepticus in Rats.The Journal of pharmacology and experimental therapeutics · 2024Article
- Promising therapeutic effects of high-frequency repetitive transcranial magnetic stimulation (HF-rTMS) in addressing autism spectrum disorder induced by valproic acid.Frontiers in neuroscience · 2024Article
- Exploring the association of disease-modifying therapies for multiple sclerosis and BTK inhibitors with epilepsy.Therapeutic advances in neurological disorders · 2024Article
- Mice deficient in complement C3 are protected against recognition memory deficits and astrogliosis induced by status epilepticus.Frontiers in molecular neuroscience · 2023Article
- Constitutively active microglial populations limit anorexia induced by the food contaminant deoxynivalenol.Journal of neuroinflammation · 2022Article
- Circulating neurofilament light chain as a promising biomarker of AAV-induced dorsal root ganglia toxicity in nonclinical toxicology species.Molecular therapy. Methods & clinical development · 2022Article
- Sleep Disruption Worsens Seizures: Neuroinflammation as a Potential Mechanistic Link.International journal of molecular sciences · 2021Review
- Hit by a Smooth CD8: T-Cell Attack on Hippocampal Neurons Triggers Limbic Encephalitis and Epilepsy.Epilepsy currents · 2021Article
- Fibroblast Growth Factor 9 Stimulates Neuronal Length Through NF-kB Signaling in Striatal Cell Huntington's Disease Models.Molecular neurobiology · 2021Article
- Aberrant Complement System Activation in Neurological Disorders.International journal of molecular sciences · 2021Review
- Neuroinflammation as a Therapeutic Target for Mitigating the Long-Term Consequences of Acute Organophosphate Intoxication.Frontiers in pharmacology · 2021Review
- Suppression of Microgliosis With the Colony-Stimulating Factor 1 Receptor Inhibitor PLX3397 Does Not Attenuate Memory Defects During Epileptogenesis in the Rat.Frontiers in neurology · 2021Article
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7 authors.
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Abstract
Status epilepticus (SE) triggers pathological changes to hippocampal dendrites that may promote epileptogenesis. The microtubule associated protein 2 (Map2) helps stabilize microtubules of the dendritic cytoskeleton. Recently, we reported a substantial decline in Map2 that coincided with robust microglia accumulation in the CA1 hippocampal region after an episode of SE. A spatial correlation between Map2 loss and reactive microglia was also reported in human cortex from refractory epilepsy. New evidence supports that microglia modulate dendritic structures. Thus, to identify a potential association between SE-induced Map2 and microglial changes, a spatiotemporal profile of these events is necessary. We used immunohistochemistry to determine the distribution of Map2 and the microglia marker IBA1 in the hippocampus after pilocarpine-induced SE from 4 hrs to 35 days. We found a decline in Map2 immunoreactivity in the CA1 area that reached minimal levels at 14 days post-SE and partially increased thereafter. In contrast, maximal microglia accumulation occurred in the CA1 area at 14 days post-SE. Our data indicate that SE-induced Map2 and microglial changes parallel each other's spatiotemporal profiles. These findings may lay the foundation for future mechanistic studies to help identify potential roles for microglia in the dendritic pathology associated with SE and epilepsy.
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