ArticleCurrent neuropharmacology2011
Kainic Acid-induced neurotoxicity: targeting glial responses and glia-derived cytokines.
Article in Current neuropharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 2 of them syntheses that pooled it.
What it found
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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
64 citing papers in PubMed, 2 syntheses or guidelines pooled it, 139 citations in OpenAlex.
- Emerging perspectives on mitochondrial dysfunctioning and inflammation in epileptogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Pooled it
- Pooled it
- Neuroprotective Effects of Pinostrobin in a Rat Model of Kainic Acid-Induced Epilepsy.International journal of molecular sciences · 2026Article
- The Role of Pyrrolidine in Antibacterial Drug Discovery: Clinically Approved Antibiotics, Novel Derivatives, and Future Perspectives.International journal of molecular sciences · 2026Review
- Wnt activation during epileptogenesis prevents pathological immature dentate granule cell morphological changes in animal models of unilateral and bilateral temporal lobe epilepsy.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- Article
- The impact of seizures on REM sleep and the cholinergic pedunculopontine nucleus in a mouse model of Dravet Syndrome.bioRxiv : the preprint server for biology · 2026Article
- Biochanin A prevents neurodegeneration and oxidative stress in a kainic acid model of epilepsy by activating the PI3K/Akt/Nrf2 signaling pathway.Scientific reports · 2025Article
- Intrinsic brain network stability during kainic acid-induced epileptogenesis.Epilepsia open · 2025Article
- The Lateral Habenula Is Necessary for Maternal Behavior in the Naturally Parturient Primiparous Mouse Dam.eNeuro · 2025Article
- Elevated interleukin-12B is associated with increased seizure susceptibility: insights from two-sample Mendelian randomization andFrontiers in neurology · 2025Article
- Article
- (+)-Borneol inhibits neuroinflammation and M1 phenotype polarization of microglia in epileptogenesis through the TLR4-NFκB signaling pathway.Frontiers in neuroscience · 2024Article
- Glutamate Receptor Dysregulation and Platelet Glutamate Dynamics in Alzheimer's and Parkinson's Diseases: Insights into Current Medications.Biomolecules · 2023Review
- The Physio-Pathological Role of Group I Metabotropic Glutamate Receptors Expressed by Microglia in Health and Disease with a Focus on Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2023Review
- Organic Kainate Single Crystals for Second-Harmonic and Broadband THz Generation.ACS applied materials & interfaces · 2023Article
- Regulation of MAP2, GFAP, and calcium in the CA3 Region Following Kainic Acid Exposure to organotypic hippocampal slice culture.F1000Research · 2023Article
- Protocol paper: kainic acid excitotoxicity-induced spinal cord injury paraplegia in Sprague-Dawley rats.Biological research · 2022Article
- Non-invasive In Vivo Brain Astrogenesis and Astrogliosis Quantification Using a Far-red E2-Crimson Transgenic Reporter Mouse.Molecular neurobiology · 2022Article
- NMDA and AMPA Receptors at Synapses: Novel Targets for Tau and α-Synuclein Proteinopathies.Biomedicines · 2022Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glutamate excitotoxicity contributes to a variety of disorders in the central nervous system, which is triggered primarily by excessive Ca(2+) influx arising from overstimulation of glutamate receptors, followed by disintegration of the endoplasmic reticulum (ER) membrane and ER stress, the generation and detoxification of reactive oxygen species as well as mitochondrial dysfunction, leading to neuronal apoptosis and necrosis. Kainic acid (KA), a potent agonist to the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate class of glutamate receptors, is 30-fold more potent in neuro-toxicity than glutamate. In rodents, KA injection resulted in recurrent seizures, behavioral changes and subsequent degeneration of selective populations of neurons in the brain, which has been widely used as a model to study the mechanisms of neurodegenerative pathways induced by excitatory neurotransmitter. Microglial activation and astrocytes proliferation are the other characteristics of KA-induced neurodegeneration. The cytokines and other inflammatory molecules secreted by activated glia cells can modify the outcome of disease progression. Thus, anti-oxidant and anti-inflammatory treatment could attenuate or prevent KA-induced neurodegeneration. In this review, we summarized updated experimental data with regard to the KA-induced neurotoxicity in the brain and emphasized glial responses and glia-oriented cytokines, tumor necrosis factor-α, interleukin (IL)-1, IL-12 and IL-18.
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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.