ReviewFrontiers in molecular neuroscience2018
Kainate Receptors: Role in Epilepsy.
Review in Frontiers in molecular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 75 citations in OpenAlex.
- Glutamate attenuates the ILC2 response and allergic airway inflammation via the kainate receptor GluK2.Cellular & molecular immunology · 2026Article
- Ireland-Claisen Rearrangement as a Stereocontrolled Bond-Construction Strategy in Natural Product Total Synthesis.ACS omega · 2026Review
- Neto2 Phosphorylation Promotes Neuronal Loss in KA-Induced Epileptic Rat Hippocampus by Upregulating the Interaction with GluK2.Neurochemical research · 2026Article
- Glutamatergic Neurotransmission Disruption as a Pathomechanism of Brain Damage in Disorders of Amino Acid and Organic Acid Metabolism: Insights from Animal and Cellular Studies.Neurochemical research · 2026Review
- The Role of GABA and Its Receptors in Temporal Lobe Epilepsy.Biomolecules · 2026Review
- Model-Dependent Attenuation of Seizures by Cinnabar.Neuroscience bulletin · 2026Article
- Effects of Troxerutin on Oxidative Stress, Inflammation and Galectin- 3 Expression in Intracerebroventricular Kainic Acid-Induced Neurotoxicity.Inflammation · 2025Article
- Structure and gating of kainate receptors.Frontiers in pharmacology · 2025Review
- Increased GluK1 Subunit Receptors in Corticostriatal Projection from the Anterior Cingulate Cortex Contributed to Seizure-Like Activities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Familial Alzheimer's Disease Neurons Bearing Mutations inLife (Basel, Switzerland) · 2024Article
- Altered neurological and neurobehavioral phenotypes in a mouse model of the recurrent KCNB1-p.R306C voltage-sensor variant.Neurobiology of disease · 2024Article
- Gene Expression at the Tripartite Synapse: Bridging the Gap Between Neurons and Astrocytes.Advances in neurobiology · 2024Review
- Article
- Enhanced Membrane Incorporation of H289Y Mutant GluK1 Receptors from the Audiogenic Seizure-Prone GASH/Sal Model: Functional and Morphological Impacts onInternational journal of molecular sciences · 2023Article
- Sigma-1 receptor and seizures.Pharmacological research · 2023Review
- The Role of Glutamate Receptors in Epilepsy.Biomedicines · 2023Review
- Identification of a Novel Idiopathic Epilepsy Risk Locus and a Variant in theAnimals : an open access journal from MDPI · 2023Article
- Kainate receptors in the CA2 region of the hippocampus.Neural regeneration research · 2023Article
- Kainate Receptor Antagonists: Recent Advances and Therapeutic Perspective.International journal of molecular sciences · 2023Review
- Efavirenz restored NMDA receptor dysfunction and inhibited epileptic seizures inFrontiers in neuroscience · 2023Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kainate (KA) is a potent neurotoxin that has been widely used experimentally to induce acute brain seizures and, after repetitive treatments, as a chronic model of temporal lobe epilepsy (TLE), with similar features to those observed in human patients with TLE. However, whether KA activates KA receptors (KARs) as an agonist to mediate the induction of acute seizures and/or the chronic phase of epilepsy, or whether epileptogenic effects of the neurotoxin are indirect and/or mediated by other types of receptors, has yet to be satisfactorily elucidated. Positing a direct involvement of KARs in acute seizures induction, as well as a direct pathophysiological role of KARs in the chronic phase of TLE, recent studies have examined the specific subunit compositions of KARs that might underly epileptogenesis. In the present mini-review, we discuss the use of KA as a convulsant in the experimental models of acute seizures of TLE, and consider the involvement of KARs, their subunit composition and the mode of action in KAR-mediated epilepsy. In acute models, evidence points to epileptogenesis being precipitated by an overall depression of interneuron GABAergic transmission mediated by GluK1 containing KARs. On glutamatergic principal cell in the hippocampus, GluK2-containing KARs regulate post-synaptic excitability and susceptibility to KA-mediated epileptogenesis. In chronic models, a role GluK2-containing KARs in the hippocampal CA3 region provokes limbic seizures. Also observed in the hippocampus, is a 'reactive plasticity', where MF sprouting is seen with target granule cells at aberrant synapses recruiting
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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.