ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Ca(V)1.3-driven SK channel activation regulates pacemaking and spike frequency adaptation in mouse chromaffin cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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40 citing papers in PubMed, 68 citations in OpenAlex.
- Reduced SK channel control of mesolimbic dopamine neuron firing drives reward seeking adaptations in chronic pain.bioRxiv : the preprint server for biology · 2025Article
- Adaptive remodeling of rat adrenomedullary stimulus-secretion coupling in a chronic hypertensive environment.Cellular and molecular life sciences : CMLS · 2024Article
- Kinetics and functional consequences of BK channels activation by N-type CaFrontiers in cellular neuroscience · 2024Article
- The human channel gating-modifying A749G CACNA1D (Cav1.3) variant induces a neurodevelopmental syndrome-like phenotype in mice.JCI insight · 2023Article
- Two firing modes and well-resolved NaPflugers Archiv : European journal of physiology · 2023Article
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- Pro-arrhythmogenic effects ofParasitology · 2021Article
- Role of High Voltage-Gated CaCells · 2021Review
- Fast inactivation of Nav1.3 channels by FGF14 proteins: An unconventional way to regulate the slow firing of adrenal chromaffin cells.The Journal of general physiology · 2021Article
- Nav1.3 and FGF14 are primary determinants of the TTX-sensitive sodium current in mouse adrenal chromaffin cells.The Journal of general physiology · 2021Article
- Fast inactivation of Nav current in rat adrenal chromaffin cells involves two independent inactivation pathways.The Journal of general physiology · 2021Article
- A sodium background conductance controls the spiking pattern of mouse adrenal chromaffin cells in situ.The Journal of physiology · 2021Article
- Cav1.2 channelopathies causing autism: new hallmarks on Timothy syndrome.Pflugers Archiv : European journal of physiology · 2020Review
- Na/Ca exchange in the atrium: Role in sinoatrial node pacemaking and excitation-contraction coupling.Cell calcium · 2020Review
- Small and Intermediate Calcium Activated Potassium Channels in the Heart: Role and Strategies in the Treatment of Cardiovascular Diseases.Frontiers in physiology · 2020Review
- Chromaffin Cells of the Adrenal Medulla: Physiology, Pharmacology, and Disease.Comprehensive Physiology · 2019Article
- Selective attenuation of Ether-a-go-go related KeLife · 2019Article
- Impaired chromaffin cell excitability and exocytosis in autistic Timothy syndrome TS2-neo mouse rescued by L-type calcium channel blockers.The Journal of physiology · 2019Article
- Quantal Release of Dopamine and Action Potential Firing Detected in Midbrain Neurons by Multifunctional Diamond-Based Microarrays.Frontiers in neuroscience · 2019Article
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Authors and funding
4 authors at 3 institutions in 3 countries.
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Abstract
Mouse chromaffin cells (MCCs) fire spontaneous action potentials (APs) at rest. Ca(v)1.3 L-type calcium channels sustain the pacemaker current, and their loss results in depolarized resting potentials (V(rest)), spike broadening, and remarkable switches into depolarization block after BayK 8644 application. A functional coupling between Ca(v)1.3 and BK channels has been reported but cannot fully account for the aforementioned observations. Here, using Ca(v)1.3(-/-) mice, we investigated the role of Ca(v)1.3 on SK channel activation and how this functional coupling affects the firing patterns induced by sustained current injections. MCCs express SK1-3 channels whose tonic currents are responsible for the slow irregular firing observed at rest. Percentage of frequency increase induced by apamin was found inversely correlated to basal firing frequency. Upon stimulation, MCCs build-up Ca(v)1.3-dependent SK currents during the interspike intervals that lead to a notable degree of spike frequency adaptation (SFA). The major contribution of Ca(v)1.3 to the subthreshold Ca(2+) charge during an AP-train rather than a specific molecular coupling to SK channels accounts for the reduced SFA of Ca(v)1.3(-/-) MCCs. Low adaptation ratios due to reduced SK activation associated with Ca(v)1.3 deficiency prevent the efficient recovery of Na(V) channels from inactivation. This promotes a rapid decline of AP amplitudes and facilitates early onset of depolarization block following prolonged stimulation. Thus, besides serving as pacemaker, Ca(v)1.3 slows down MCC firing by activating SK channels that maintain Na(V) channel availability high enough to preserve stable AP waveforms, even upon high-frequency stimulation of chromaffin cells during stress responses.
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