ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019
Protein Kinase A-Mediated Suppression of the Slow Afterhyperpolarizing KCa3.1 Current in Temporal Lobe Epilepsy.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 25 citations in OpenAlex.
- Local targeted suppression of neocortical spreading depolarization amplitude by viral expression of KCa3.1 channels.Gene therapy · 2026Article
- Leukocytes Transcriptome Analysis of Genes Associated with Epilepsy Duration and Age of Onset.Molecular neurobiology · 2026Article
- Calcium-Activated Potassium Channel KMolecular neurobiology · 2025Article
- Overexpression of KCNN4 channels in principal neurons produces an anti-seizure effect without reducing their coding ability.Gene therapy · 2024Article
- Vasoactive intestinal peptide excites GnRH neurons via KCa3.1, a potential player in the slow afterhyperpolarization current.Frontiers in cellular neuroscience · 2024Article
- Corticotropin Releasing Factor Mediates KThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Regulatory role of KCa3.1 in immune cell function and its emerging association with rheumatoid arthritis.Frontiers in immunology · 2022Review
- Chemical modulation of Kv7 potassium channels.RSC medicinal chemistry · 2021Review
- PKA-RIIβ autophosphorylation modulates PKA activity and seizure phenotypes in mice.Communications biology · 2021Article
- ATP-evoked intracellular CaJournal of neuroinflammation · 2021Article
- Behavioral Deficits in Mice with Postnatal Disruption ofCerebral cortex communications · 2021Article
- The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons.Frontiers in physiology · 2021Review
- Activation of cyclin-dependent kinase 5 broadens action potentials in human sensory neurons.Molecular painArticle
- KCa3.1 Impairment Is Not Just a Slow Afterthought in Epilepsy.Epilepsy currentsArticle
- Phyllathin From Phyllanthus Amarus Ameliorates Epileptic Convulsion and Kindling Associated Post-Ictal Depression in Mice via Inhibition of NF-κB/TLR-4 Pathway.Dose-response : a publication of International Hormesis SocietyArticle
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4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Brain insults, such as trauma, stroke, anoxia, and status epilepticus (SE), cause multiple changes in synaptic function and intrinsic properties of surviving neurons that may lead to the development of epilepsy. Experimentally, a single SE episode, induced by the convulsant pilocarpine, initiates the development of an epileptic condition resembling human temporal lobe epilepsy (TLE). Principal hippocampal neurons from such epileptic animals display enhanced spike output in response to excitatory stimuli compared with neurons from nonepileptic animals. This enhanced firing is negatively related to the size of the slow afterhyperpolarization (sAHP), which is reduced in the epileptic neurons. The sAHP is an intrinsic neuronal negative feedback mechanism consisting normally of two partially overlapping components produced by disparate mechanisms. One component is generated by activation of Ca
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