ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Loss of Cav1.3 channels reveals the critical role of L-type and BK channel coupling in pacemaking mouse adrenal chromaffin cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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Who cites it
97 citing papers in PubMed, 180 citations in OpenAlex.
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- HCN1 is a primary HCN Pacemaker Channel in Neurons.Nature communications · 2026Article
- Inhibitory Activity of Calcium and Sodium Ion Channels of NeurotoxicPharmaceuticals (Basel, Switzerland) · 2025Article
- CaMKII clusters neuronal LTCCs in biomolecular condensates to gate excitation-transcription coupling.bioRxiv : the preprint server for biology · 2025Article
- Roles for PKC signaling in chromaffin cell exocytosis.Biophysical journal · 2025Article
- Adaptive remodeling of rat adrenomedullary stimulus-secretion coupling in a chronic hypertensive environment.Cellular and molecular life sciences : CMLS · 2024Article
- Cellular mechanisms underlying pituitary adenylate cyclase activating polypeptide-stimulated secretion in the adrenal medulla.Biochemical Society transactions · 2024Review
- A genetically encoded actuator boosts L-type calcium channel function in diverse physiological settings.Science advances · 2024Article
- The L-type calcium channel CaV1.3: A potential target for cancer therapy.Journal of cellular and molecular medicine · 2024Review
- Modulating CaBiophysical journal · 2024Article
- A PACAP-activated network for secretion requires coordination of CaMolecular biology of the cell · 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
- CaBritish journal of pharmacology · 2023Review
- PACAP and acetylcholine cause distinct Ca2+ signals and secretory responses in chromaffin cells.The Journal of general physiology · 2023Article
- Two firing modes and well-resolved NaPflugers Archiv : European journal of physiology · 2023Article
- Article
- CACNA1D-Related Channelopathies: From Hypertension to Autism.Handbook of experimental pharmacology · 2023Review
- DisruptedProceedings of the National Academy of Sciences of the United States of America · 2022Article
37 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
We studied wild-type (WT) and Cav1.3(-/-) mouse chromaffin cells (MCCs) with the aim to determine the isoform of L-type Ca(2+) channel (LTCC) and BK channels that underlie the pacemaker current controlling spontaneous firing. Most WT-MCCs (80%) were spontaneously active (1.5 Hz) and highly sensitive to nifedipine and BayK-8644 (1,4-dihydro-2,6-dimethyl-5-nitro-4-[2-(trifluoromethyl)phenyl]-3-pyridinecarboxylic acid, methyl ester). Nifedipine blocked the firing, whereas BayK-8644 increased threefold the firing rate. The two dihydropyridines and the BK channel blocker paxilline altered the shape of action potentials (APs), suggesting close coupling of LTCCs to BK channels. WT-MCCs expressed equal fractions of functionally active Cav1.2 and Cav1.3 channels. Cav1.3 channel deficiency decreased the number of normally firing MCCs (30%; 2.0 Hz), suggesting a critical role of these channels on firing, which derived from their slow inactivation rate, sizeable activation at subthreshold potentials, and close coupling to fast inactivating BK channels as determined by using EGTA and BAPTA Ca(2+) buffering. By means of the action potential clamp, in TTX-treated WT-MCCs, we found that the interpulse pacemaker current was always net inward and dominated by LTCCs. Fast inactivating and non-inactivating BK currents sustained mainly the afterhyperpolarization of the short APs (2-3 ms) and only partially the pacemaker current during the long interspike (300-500 ms). Deletion of Cav1.3 channels reduced drastically the inward Ca(2+) current and the corresponding Ca(2+)-activated BK current during spikes. Our data highlight the role of Cav1.3, and to a minor degree of Cav1.2, as subthreshold pacemaker channels in MCCs and open new interesting features about their role in the control of firing and catecholamine secretion at rest and during sustained stimulations matching acute stress.
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