ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Control of spontaneous firing patterns by the selective coupling of calcium currents to calcium-activated potassium currents in striatal cholinergic interneurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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90 citing papers in PubMed, 167 citations in OpenAlex.
- Morphoelectric Diversity and Specialization of Neuronal Cell Types in the Primate Striatum.bioRxiv : the preprint server for biology · 2026Article
- Regional heterogeneity of striatal cholinergic interneurons: setting the stage for diverse behavioral repertoires.Frontiers in cellular neuroscience · 2026Review
- Levodopa Disrupts Activity Patterns and Encoding of Movement in Striatal Cholinergic Interneurons of Behaving Mice.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- Extrinsic and intrinsic control of striatal cholinergic interneuron activity.Frontiers in molecular neuroscience · 2025Review
- Rapid modulation of striatal cholinergic interneurons and dopamine release by satellite astrocytes.Nature communications · 2024Article
- Corticotropin releasing factor alters the functional diversity of accumbal cholinergic interneurons.Journal of neurophysiology · 2024Article
- Regional heterogeneity in the membrane properties of mouse striatal neurons.Frontiers in cellular neuroscience · 2024Article
- Large conductance voltage-and calcium-activated KFrontiers in pharmacology · 2024Review
- Cognitive effects of thalamostriatal degeneration are ameliorated by normalizing striatal cholinergic activity.Science advances · 2023Article
- ACh Transfers: Homeostatic Plasticity of Cholinergic Synapses.Cellular and molecular neurobiology · 2023Review
- A spiking computational model for striatal cholinergic interneurons.Brain structure & function · 2023Article
- Motor deficit and lack of overt dystonia in Dlx conditional Dyt1 knockout mice.Behavioural brain research · 2023Article
- CaInternational journal of molecular sciences · 2023Review
- Striatal CDK5 Regulates Cholinergic Neuron Activation and Dyskinesia-like Behaviors through BK Channels.Research (Washington, D.C.) · 2023Article
- Developmental regulation of thalamus-driven pauses in striatal cholinergic interneurons.iScience · 2022Article
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- Electrophysiological characterization of the striatal cholinergic interneurons inDystonia (Lausanne, Switzerland) · 2022Article
- Synaptic determinants of cholinergic interneurons hyperactivity during parkinsonism.Frontiers in synaptic neuroscience · 2022Article
- A familiar study on self-limited childhood epilepsy patients using hIPSC-derived neurons shows a bias towards immaturity at the morphological, electrophysiological and gene expression levels.Stem cell research & therapy · 2021Article
30 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 1 country.
Funding
Abstract
The spontaneous firing patterns of striatal cholinergic interneurons are sculpted by potassium currents that give rise to prominent afterhyperpolarizations (AHPs). Large-conductance calcium-activated potassium (BK) channel currents contribute to action potential (AP) repolarization; small-conductance calcium-activated potassium channel currents generate an apamin-sensitive medium AHP (mAHP) after each AP; and bursts of APs generate long-lasting slow AHPs (sAHPs) attributable to apamin-insensitive currents. Because all these currents are calcium dependent, we conducted voltage- and current-clamp whole-cell recordings while pharmacologically manipulating calcium channels of the plasma membrane and intracellular stores to determine what sources of calcium activate the currents underlying AP repolarization and the AHPs. The Cav2.2 (N-type) blocker omega-conotoxin GVIA (1 microM) was the only blocker that significantly reduced the mAHP, and it induced a transition to rhythmic bursting in one-third of the cells tested. Cav1 (L-type) blockers (10 microM dihydropyridines) were the only ones that significantly reduced the sAHP. When applied to cells induced to burst with apamin, dihydropyridines reduced the sAHPs and abolished bursting. Depletion of intracellular stores with 10 mM caffeine also significantly reduced the sAHP current and reversibly regularized firing. Application of 1 microM omega-conotoxin MVIIC (a Cav2.1/2.2 blocker) broadened APs but had a negligible effect on APs in cells in which BK channels were already blocked by submillimolar tetraethylammonium chloride, indicating that Cav2.1 (Q-type) channels provide the calcium to activate BK channels that repolarize the AP. Thus, calcium currents are selectively coupled to the calcium-dependent potassium currents underlying the AHPs, thereby creating mechanisms for control of the spontaneous firing patterns of these neurons.
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