ArticleJournal of neurophysiology2011
Inhibition of Ca2+-activated large-conductance K+ channel activity alters synaptic AMPA receptor phenotype in mouse cerebellar stellate cells.
Article in Journal of neurophysiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Emotional stress increases GluA2 expression and potentiates fear memory via adenylyl cyclase 5.Cell reports · 2025Article
- CaInternational journal of molecular sciences · 2023Review
- Bursting in cerebellar stellate cells induced by pharmacological agents: Non-sequential spike adding.PLoS computational biology · 2020Article
- +mRNA expression of LRRC55 protein (leucine-rich repeat-containing protein 55) in the adult mouse brain.PloS one · 2018Article
- Temporal integration and 1/Journal of neurophysiology · 2017Article
- Topological Regulation of Synaptic AMPA Receptor Expression by the RNA-Binding Protein CPEB3.Cell reports · 2016Article
- Overexpression of the Large-Conductance, Ca2+-Activated K+ (BK) Channel Shortens Action Potential Duration in HL-1 Cardiomyocytes.PloS one · 2015Article
- Upregulation of cystathionine-β-synthetase expression contributes to inflammatory pain in rat temporomandibular joint.Molecular pain · 2014Article
- Ethanol modulation of mammalian BK channels in excitable tissues: molecular targets and their possible contribution to alcohol-induced altered behavior.Frontiers in physiology · 2014Review
- A role of TARPs in the expression and plasticity of calcium-permeable AMPARs: evidence from cerebellar neurons and glia.Neuropharmacology · 2013Review
- Hydrogen sulfide increases excitability through suppression of sustained potassium channel currents of rat trigeminal ganglion neurons.Molecular pain · 2013Article
- Ca(2+) permeable AMPA receptors switch allegiances: mechanisms and consequences.The Journal of physiology · 2012Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Many fast-spiking inhibitory interneurons, including cerebellar stellate cells, fire brief action potentials and express α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-type glutamate receptors (AMPAR) that are permeable to Ca(2+) and do not contain the GluR2 subunit. In a recent study, we found that increasing action potential duration promotes GluR2 gene transcription in stellate cells. We have now tested the prediction that activation of potassium channels that control the duration of action potentials can suppress the expression of GluR2-containing AMPARs at stellate cell synapses. We find that large-conductance Ca(2+)-activated potassium (BK) channels mediate a large proportion of the depolarization-evoked noninactivating potassium current in stellate cells. Pharmacological blockade of BK channels prolonged the action potential duration in postsynaptic stellate cells and altered synaptic AMPAR subtype from GluR2-lacking to GluR2-containing Ca(2+)-impermeable AMPARs. An L-type channel blocker abolished an increase in Ca(2+) entry that was associated with spike broadening and also prevented the BK channel blocker-induced switch in AMPAR phenotype. Thus blocking BK potassium channels prolongs the action potential duration and increases the expression of GluR2-containing receptors at the synapse by enhancing Ca(2+) entry in cerebellar stellate cells.
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Registered trials
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