ReviewExpert opinion on therapeutic targets2011
Targeting BK (big potassium) channels in epilepsy.
Review in Expert opinion on therapeutic targets, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
45 citing papers in PubMed, 87 citations in OpenAlex.
- Involvement of BK Channels and Ryanodine Receptors in Salicylate-induced Tinnitus.Molecular neurobiology · 2025Article
- Large conductance voltage-and calcium-activated KFrontiers in pharmacology · 2024Review
- The sulfonadyns: a class of aryl sulfonamides inhibiting dynamin I GTPase and clathrin mediated endocytosis are anti-seizure in animal models.RSC medicinal chemistry · 2023Article
- A Targeted, Low-Throughput Compound Screen in aeNeuro · 2023Article
- KCurrent neuropharmacology · 2023Review
- Multi-modal characterization and simulation of human epileptic circuitry.Cell reports · 2022Article
- Development of charybdotoxin Q18F variant as a selective peptide blocker of neuronal BK(α + β4) channel for the treatment of epileptic seizures.Protein science : a publication of the Protein Society · 2022Article
- Neuronal mechanism of a BK channelopathy in absence epilepsy and dyskinesia.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Small molecule modulation of the large-conductance calcium-activated potassium channel suppresses salicylate-induced tinnitus in mice.Frontiers in neuroscience · 2022Article
- Rapid volume pulsation of the extracellular space coincides with epileptiform activity in mice and depends on the NBCe1 transporter.The Journal of physiology · 2021Article
- The Large-Conductance, Calcium-Activated Potassium Channel: A Big Key Regulator of Cell Physiology.Frontiers in physiology · 2021Review
- Article
- Identification of common genetic markers of paroxysmal neurological disorders using a network analysis approach.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2020Article
- Fluorogen activating protein toolset for protein trafficking measurements.Traffic (Copenhagen, Denmark) · 2020Review
- Astrocytes as Guardians of Neuronal Excitability: Mechanisms Underlying Epileptogenesis.Frontiers in neurology · 2020Review
- BK ablation attenuates osteoblast bone formation via integrin pathway.Cell death & disease · 2019Article
- The Cannabinoid-Like Compound, VSN16R, Acts on Large Conductance, CaPharmaceuticals (Basel, Switzerland) · 2019Article
- Functional Connectivity of the Parasubiculum and Its Role in Temporal Lobe Epilepsy.Neuroscience · 2019Article
- Ion channel dysfunction in cerebellar ataxia.Neuroscience letters · 2019Review
- Chronic glucocorticoid exposure activates BK-NLRP1 signal involving in hippocampal neuron damage.Journal of neuroinflammation · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
introductionEpilepsies are disorders of neuronal excitability characterized by spontaneous and recurrent seizures. Ion channels are critical for regulating neuronal excitability and, therefore, can contribute significantly to epilepsy pathophysiology. In particular, large conductance, Ca2+-activated K+ (BKCa) channels play an important role in seizure etiology. These channels are activated by both membrane depolarization and increased intracellular Ca2+. This unique coupling of Ca2+ signaling to membrane depolarization is important in controlling neuronal hyperexcitability, as outward K+ current through BKCa channels hyperpolarizes neurons. AREAS COVERED: BKCa channel structure-function and the role of these channels in epilepsy pathophysiology. EXPERT OPINION: Loss-of-function BKCa channel mutations contribute to neuronal hyperexcitability that can lead to temporal lobe epilepsy, tonic-clonic seizures and alcohol withdrawal seizures. Similarly, BKCa channel blockade can trigger seizures and status epilepticus. Paradoxically, some mutations in BKCa channel subunit can give rise to channel gain-of-function that leads to development of idiopathic epilepsy (primarily absence epilepsy). Seizures themselves also enhance BKCa channel currents associated with neuronal hyperexcitability, and blocking BKCa channels suppresses generalized tonic-clonic seizures. Thus, both loss-of-function and gain-of-function BKCa channels might serve as molecular targets for drugs to suppress certain seizure phenotypes including temporal lobe seizures and absence seizures, respectively.
Indexed as
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What OpenQuestion holds
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.