ArticleNeurobiology of disease2015
KCC2 function modulates in vitro ictogenesis.
Article in Neurobiology of disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 72 citations in OpenAlex.
- Neuron-derived neurotrophic factor-positive interneurons: a cellular target for anti-seizure therapies.EBioMedicine · 2026Article
- Enhancing KCC2 function reduces interictal activity and prevents seizures in temporal lobe epilepsy.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Acceleration of axonal regeneration by GABA/Gly excitation.Anatomical science international · 2026Review
- Article
- Spinal KCC2 Mediates the Modulation Effect of HDAC2 on Bone Cancer Pain in Rats.Current cancer drug targets · 2026Article
- WONOEP XVII appraisal: Targeting network excitability beyond the synapse -Neurotransmitter, ionic, and electro -diffusions.Epilepsia · 2025Review
- To reveal biomarkers related to macrophage and lactic acid metabolism in renal fibrosis and explore their mechanisms.Frontiers in immunology · 2025Article
- Neuronal KActa pharmacologica Sinica · 2024Review
- Reduced Cholecystokinin-Expressing Interneuron Input Contributes to Disinhibition of the Hippocampal CA2 Region in a Mouse Model of Temporal Lobe Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Focal seizures are organized by feedback between neural activity and ion concentration changes.eLife · 2022Article
- Inhibiting with-no-lysine kinases enhances K+/Cl- cotransporter 2 activity and limits status epilepticus.Brain : a journal of neurology · 2022Article
- Targeting ischemia-induced KCC2 hypofunction rescues refractory neonatal seizures and mitigates epileptogenesis in a mouse model.Science signaling · 2021Article
- Targeting the WNK-SPAK/OSR1 Pathway and Cation-Chloride Cotransporters for the Therapy of Stroke.International journal of molecular sciences · 2021Review
- Dysregulation of GABAergic Signaling in Neurodevelomental Disorders: Targeting Cation-Chloride Co-transporters to Re-establish a Proper E/I Balance.Frontiers in cellular neuroscience · 2021Review
- Article
- Intracellular ClPflugers Archiv : European journal of physiology · 2020Review
- Traumatic Brain Injury Temporal Proteome Guides KCC2-Targeted Therapy.Journal of neurotrauma · 2019Article
- Ionic and synaptic mechanisms of seizure generation and epileptogenesis.Neurobiology of disease · 2019Review
- KCC2 overexpression prevents the paradoxical seizure-promoting action of somatic inhibition.Nature communications · 2019Article
- Role of NKCC1 and KCC2 in Epilepsy: From Expression to Function.Frontiers in neurology · 2019Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
GABAA receptor-mediated inhibition is active and may contribute to epileptiform synchronization. The efficacy of inhibition relies on low levels of intracellular Cl(-), which are controlled by KCC2 activity. This evidence has led us to analyze with field potential recordings the effects induced by the KCC2 blockers VU0240551 (10 μM) or bumetanide (50 μM) and by the KCC2 enhancer CLP257 (100 μM) on the epileptiform discharges generated by piriform and entorhinal cortices (PC and EC, respectively) in an in vitro brain slice preparation. Ictal- and interictal-like discharges along with high-frequency oscillations (HFOs, ripples: 80-200 Hz, fast ripples: 250-500 Hz) were recorded from these two regions during application of 4-aminopyridine (4AP, 50 μM). Blocking KCC2 activity with either VU024055 or high doses of bumetanide abolished ictal discharge in both PC and EC; in addition, these experimental procedures decreased the interval of occurrence and duration of interictal discharges. In contrast, enhancing KCC2 activity with CLP257 increased ictal discharge duration in both regions. Finally, blocking KCC2 activity decreased the duration and amplitude of pharmacologically isolated synchronous GABAergic events whereas enhancing KCC2 activity led to an increase in their duration. Our data demonstrate that in vitro ictogenesis is abolished or facilitated by inhibiting or enhancing KCC2 activity, respectively. We propose that these effects may result from the reduction of GABAA receptor-dependent increases in extracellular K(+) that are known to rest on KCC2 function.
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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.