ArticleChannels (Austin, Tex.)
Are Ca(v)1.3 pacemaker channels in chromaffin cells? Possible bias from resting cell conditions and DHP blockers usage.
Article in Channels (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Cav1.2 channelopathies causing autism: new hallmarks on Timothy syndrome.Pflugers Archiv : European journal of physiology · 2020Review
- Chromaffin Cells of the Adrenal Medulla: Physiology, Pharmacology, and Disease.Comprehensive Physiology · 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
- Two central pattern generators from the crab,eLife · 2018Article
- Roles of NaPflugers Archiv : European journal of physiology · 2018Review
- L-type calcium channels in exocytosis and endocytosis of chromaffin cells.Pflugers Archiv : European journal of physiology · 2018Review
- New gain-of-function mutation shows CACNA1D as recurrently mutated gene in autism spectrum disorders and epilepsy.Human molecular genetics · 2017Article
- Low pHThe Journal of physiology · 2017Article
- Differential Roles for L-Type Calcium Channel Subtypes in Alcohol Dependence.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Article
- Leptin-mediated ion channel regulation: PI3K pathways, physiological role, and therapeutic potential.Channels (Austin, Tex.) · 2016Review
- Reduced availability of voltage-gated sodium channels by depolarization or blockade by tetrodotoxin boosts burst firing and catecholamine release in mouse chromaffin cells.The Journal of physiology · 2015Article
- Cav1.3 Channels as Key Regulators of Neuron-Like Firings and Catecholamine Release in Chromaffin Cells.Current molecular pharmacology · 2015Review
- Cell-type-specific tuning of Cav1.3 Ca(2+)-channels by a C-terminal automodulatory domain.Frontiers in cellular neuroscience · 2015Article
- Pyrimidine-2,4,6-triones are a new class of voltage-gated L-type Ca2+ channel activators.Nature communications · 2014Article
- Ca(V)1.3-driven SK channel activation regulates pacemaking and spike frequency adaptation in mouse chromaffin cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Equal sensitivity of Cav1.2 and Cav1.3 channels to the opposing modulations of PKA and PKG in mouse chromaffin cells.The Journal of physiology · 2012Article
- Functional chromaffin cell plasticity in response to stress: focus on nicotinic, gap junction, and voltage-gated Ca2+ channels.Journal of molecular neuroscience : MN · 2012Review
- Structural determinants of CaV1.3 L-type calcium channel gating.Channels (Austin, Tex.)Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mouse and rat chromaffin cells (MCCs, RCCs) fire spontaneously at rest and their activity is mainly supported by the two L-type Ca(2+) channels expressed in these cells (Ca(v)1.2 and Ca(v)1.3). Using Ca(v)1.3(-/-) KO MCCs we have shown that Ca(v)1.3 possess all the prerequisites for carrying subthreshold currents that sustain low frequency cell firing near resting (0.5 to 2 Hz at -50 mV): low-threshold and steep voltage dependence of activation, slow and incomplete inactivation during pulses of several hundreds of milliseconds. Ca(v)1.2 contributes also to pacemaking MCCs and possibly even Na(+) channels may participate in the firing of a small percentage of cells. We now show that at potentials near resting (-50 mV), Ca(v)1.3 carries equal amounts of Ca(2+) current to Ca(v)1.2 but activates at 9 mV more negative potentials. MCCs express only TTX-sensitive Na(v)1 channels that activate at 24 mV more positive potentials than Ca(v)1.3 and are fully inactivating. Their blockade prevents the firing only in a small percentage of cells (13%). This suggests that the order of importance with regard to pacemaking MCCs is: Ca(v)1.3, Ca(v)1.2 and Na(v)1. The above conclusions, however, rely on the proper use of DHPs, whose blocking potency is strongly holding potential dependent. We also show that small increases of KCl concentration steadily depolarize the MCCs causing abnormally increased firing frequencies, lowered and broadened AP waveforms and an increased facility of switching "non-firing" into "firing" cells that may lead to erroneous conclusions about the role of Ca(v)1.3 and Ca(v)1.2 as pacemaker channels in MCCs.
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