ArticleBrain research2010
Altered expression and function of small-conductance (SK) Ca(2+)-activated K+ channels in pilocarpine-treated epileptic rats.
Article in Brain research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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.
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Who cites it
24 citing papers in PubMed, 46 citations in OpenAlex.
- Magnesium Ions as Modulators of Voltage-Gated and Ligand-Gated Ion Channels in Central Neurons.International journal of molecular sciences · 2025Review
- Calcium-Activated Potassium Channel KMolecular neurobiology · 2025Article
- Modulation of dorsal hippocampal SK2 channels regulates morphine-enhanced neuronal oscillations and morphine-induced contextual memory encoding and retrieval.Scientific reports · 2025Article
- Human iPSC-derived glutamatergic neurons with pathogenic KCNQ2 variants display hyperactive bursting phenotypes.Neurobiology of disease · 2025Article
- KCurrent neuropharmacology · 2023Review
- Physiology and Therapeutic Potential of SK, H, and M Medium AfterHyperPolarization Ion Channels.Frontiers in molecular neuroscience · 2021Review
- Molecular Choreography and Structure of CaMembranes · 2020Review
- SK2 channel regulation of neuronal excitability, synaptic transmission, and brain rhythmic activity in health and diseases.Biochimica et biophysica acta. Molecular cell research · 2020Review
- Interstitial ions: A key regulator of state-dependent neural activity?Progress in neurobiology · 2020Review
- Activation of small conductance calcium-activated potassium channels suppresses seizure susceptibility in the genetically epilepsy-prone rats.Neuropharmacology · 2020Article
- Transcriptional Regulation of Channelopathies in Genetic and Acquired Epilepsies.Frontiers in cellular neuroscience · 2019Review
- Physiological Roles and Therapeutic Potential of CaFrontiers in molecular neuroscience · 2018Review
- SK channels participate in the formation of after burst hyperpolarization and partly inhibit the burst strength of epileptic ictal discharges.Molecular medicine reports · 2018Article
- Potassium Channels in Epilepsy.Cold Spring Harbor perspectives in medicine · 2016Review
- Article
- Homeostasis or channelopathy? Acquired cell type-specific ion channel changes in temporal lobe epilepsy and their antiepileptic potential.Frontiers in physiology · 2015Review
- Pharmacological gating modulation of small- and intermediate-conductance Ca(2+)-activated K(+) channels (KCa2.x and KCa3.1).Channels (Austin, Tex.) · 2015Review
- Overexpression of KCNN3 results in sudden cardiac death.Cardiovascular research · 2014Article
- Endothelial small-conductance and intermediate-conductance KCa channels: an update on their pharmacology and usefulness as cardiovascular targets.Journal of cardiovascular pharmacology · 2013Review
- Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Small conductance calcium (Ca(2+)) activated SK channels are critical regulators of neuronal excitability in hippocampus. Accordingly, these channels are thought to play a key role in controlling neuronal activity in acute models of epilepsy. In this study, we investigate the expression and function of SK channels in the pilocarpine model of mesial temporal lobe epilepsy. For this purpose, protein expression was assessed using western blotting assays and gene expression was analyzed using TaqMan-based probes and the quantitative real-time polymerase chain reaction (qPCR) comparative method delta-delta cycle threshold ( big up tri, open big up tri, openCT) in samples extracted from control and epileptic rats. In addition, the effect of SK channel antagonist UCL1684 and agonist NS309 on CA1 evoked population spikes was studied in hippocampal slices. Western blotting analysis showed a significant reduction in the expression of SK1 and SK2 channels at 10days following status epilepticus (SE), but levels recovered at 1month and at more than 2months after SE. In contrast, a significant down-regulation of SK3 channels was detected after 10days of SE. Analysis of gene expression by qPCR revealed a significant reduction of transcripts for SK2 (Kcnn1) and SK3 (Kcnn3) channels as early as 10days following pilocarpine-induced SE and during the chronic phase of the pilocarpine model. Moreover, bath application of UCL1684 (100nM for 15min) induced a significant increase of the population spike amplitude and number of spikes in the hippocampal CA1 area of slices obtained control and chronic epileptic rats. This effect was obliterated by co-administration of UCL1684 with SK channel agonist NS309 (1microM). Application of NS309 failed to modify population spikes in the CA1 area of slices taken from control and epileptic rats. These data indicate an abnormal expression of SK channels and a possible dysfunction of these channels in experimental MTLE.
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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.