ArticleCNS neuroscience & therapeutics2024
The JNK Signaling Pathway Regulates Seizures Through ENT1 in Pilocarpine-Induced Epilepsy Rat Model.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Brain connectivity changes associated with acute sleep deprivation: a systematic review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Pooled it
- Neuroinflammation in Epilepsy: Biochemical and Molecular Mechanisms and Implications for Natural Product-Driven Drug Discovery.International journal of molecular sciences · 2026Review
- Calponin-3 is associated with epilepsy through the regulation of astrocyte activity.Brain pathology (Zurich, Switzerland) · 2026Article
- Genetic-Epigenetic Interplay in Epilepsy: Pathways, Biomarkers, and Epigenome-Targeted Therapies.Epigenomes · 2026Review
- Gut bacteria-derived metabolites and their implications in mental health and neurological diseases.World journal of microbiology & biotechnology · 2025Review
- Targeted miRNA Delivery in Epilepsy: Mechanisms, Advances, and Therapeutic Potential.Molecular biology reports · 2025Review
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Authors and funding
7 authors.
Funding
Abstract
objectiveThe study investigates whether the expression and function of ENT1 can be regulated by inhibiting the JNK signaling pathway, thereby altering the levels of extracellular adenosine and glutamate in neurons, and subsequently affecting the progression of epilepsy.
methodsThe adult male SD rats were randomly divided into four groups: EP + SP600125 group, EP + DMSO group, EP group, and normal control group. The expression levels of ENT1, p-JNK, and JNK in the hippocampus of rats from each experimental group were detected using Western blotting technology. The expression and localization of ENT1 and p-JNK in the CA1, CA3, and DG areas of the hippocampus were detected by immunohistochemical staining and immunofluorescence staining. Microdialysis combined with liquid chromatography-mass spectrometry was used to determine the concentrations of adenosine and glutamate in the extracellular fluid of hippocampus in each experimental group.
resultsThis study showed that the JNK-specific inhibitor SP600125 could reduce ENT1 expression and seizure intensity in experimental rats. Statistical analysis confirmed that adenosine and glutamate levels in the extracellular fluid of the hippocampus increased significantly after seizures in rats, and the JNK-specific inhibitor SP600125 could increase adenosine levels in the extracellular fluid but decrease glutamate levels. SIGNIFICANCE: The JNK-specific inhibitor SP600125 can specifically inhibit the JNK signaling pathway and reduce the expression of ENT1 transporter. The mechanism is related to the transport of adenosine from the extracellular space to the intracellular space by ENT1 during epileptic states. Inhibition of ENT1 can increase the concentration of adenosine in the extracellular fluid of the hippocampus. The increase in adenosine concentration stopped glutamate from being released and reduced the amount of glutamate in the outside of the cell.
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