ArticleFrontiers in neurology2018
Changes in the Blood-Brain Barrier Function Are Associated With Hippocampal Neuron Death in a Kainic Acid Mouse Model of Epilepsy.
Article in Frontiers in neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Commonalities in gene expression and methylation changes across two rat models of acquired epilepsy.Scientific reports · 2026Article
- Polysaccharide-rich birch sap attenuates kainic acid-induced acute seizures by suppressing TLR4/NF-κB-mediated inflammation and preserving blood-brain barrier and glutamate homeostasis.Frontiers in pharmacology · 2026Article
- The missing link: TNF-α as a unifying mechanism in methamphetamine-induced neuronal dysfunction and blood-brain barrier compromise.Journal of neuroimmunology · 2025Review
- Assessment of Mannitol-Induced Chronic Blood-Brain Barrier Dysfunction In Vivo Using Magnetic Resonance.International journal of molecular sciences · 2024Article
- Mapping dynamic molecular changes in hippocampal subregions after traumatic brain injury through spatial proteomics.Clinical proteomics · 2024Article
- In the Rat Hippocampus, Pilocarpine-Induced Status Epilepticus Is Associated with Reactive Glia and Concomitant Increased Expression of CD31, PDGFRβ, and Collagen IV in Endothelial Cells and Pericytes of the Blood-Brain Barrier.International journal of molecular sciences · 2024Article
- Expression, purification, and biochemical characterization of micro- and macroalgal kainoid synthases.Methods in enzymology · 2024Article
- Activation of TLR7-mediated autophagy increases epileptic susceptibility via reduced KIF5A-dependent GABAExperimental & molecular medicine · 2023Article
- In vivo methods for imaging blood-brain barrier function and dysfunction.European journal of nuclear medicine and molecular imaging · 2023Review
- Activated protein C in epilepsy pathophysiology.Frontiers in neuroscience · 2023Review
- Combined transcriptomics and proteomics forecast analysis for potential biomarker in the acute phase of temporal lobe epilepsy.Frontiers in neuroscience · 2023Article
- Closed-loop direct control of seizure focus in a rodent model of temporal lobe epilepsy via localized electric fields applied sequentially.Nature communications · 2022Article
- Claudin5 protects the peripheral endothelial barrier in an organ and vessel-type-specific manner.eLife · 2022Article
- High-Dose Acetaminophen Alters the Integrity of the Blood-Brain Barrier and Leads to Increased CNS Uptake of Codeine in Rats.Pharmaceutics · 2022Article
- Microvascular stabilization via blood-brain barrier regulation prevents seizure activity.Nature communications · 2022Article
- Pathophysiology of blood brain barrier dysfunction during chronic cerebral hypoperfusion in vascular cognitive impairment.Theranostics · 2022Review
- The interplay of neurovasculature and adult hippocampal neurogenesis.Neuroscience letters · 2021Review
- Blood-brain barrier dysfunction as a potential therapeutic target for neurodegenerative disorders.Archives of pharmacal research · 2021Review
- Spaceflight induces oxidative damage to blood-brain barrier integrity in a mouse model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Differential Expression of CD31 and Von Willebrand Factor on Endothelial Cells in Different Regions of the Human Brain: Potential Implications for Cerebral Malaria Pathogenesis.Brain sciences · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The kainic acid (KA)-induced epilepsy experimental model is widely used to study the mechanisms underlying this disorder. Recently, the blood-brain barrier (BBB) has become an innovative alternative treatment target for epilepsy patients. KA causes neuronal injury and BBB damage in this experimental epilepsy model but the mechanisms underlying epilepsy-related neuronal injury, autophagy, and BBB damage remain unclear. Therefore, the present study investigated the relationships among neuronal injury, the expressions of autophagy-related proteins, and changes in BBB-related proteins during the acute phase of epilepsy to further understand the mechanisms and pharmacotherapy of epilepsy. NeuN immunohistochemistry and Fluoro-Jade B (FJ-B) staining in the hippocampal CA3 region revealed that neuronal death induced by intraventricular injections of 10 μg/kg KA was greater than that induced by 3 μg/kg KA. In addition, there were transient increases in the levels of microtubule-associated protein light chain 3-II (LC3I/II) and Beclin-1, which are autophagy-related proteins involved in neuronal death, in this region 24 h after the administration of 10 μg/kg KA. There were also morphological changes in BBB-related cells such as astrocytes, endothelial cells (ECs), and tight junctions (TJs). More specifically, there was a significant increase in the activation of astrocytes 72 h after the administration of 10 μg/kg KA as well as continuous increases in the expressions of platelet endothelial cell adhesion molecule-1 (PECAM-1) and BBB-related TJ proteins (Zonula occludens-1 and Claudin-5) until 72 h after KA treatment. These results suggest that the overexpression of autophagy-related proteins and astrocytes and transient increases in the expressions of BBB-related TJ proteins may be closely related to autophagic neuronal injury. These findings provide a basis for the identification of novel therapeutic targets for patients with epilepsy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.