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Journal articles on the topic 'Calcium channels'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Triggle, David J. "Calcium, calcium channels, and calcium channel antagonists." Canadian Journal of Physiology and Pharmacology 68, no. 11 (1990): 1474–81. http://dx.doi.org/10.1139/y90-224.

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Voltage-dependent Ca2+ channels are an important pathway for Ca2+ influx in excitable cells. They also represent an important site of action for a therapeutic group of agents, the Ca2+ channel antagonists. These drugs enjoy considerable use in the cardiovascular area including angina, some arrhythmias, hypertension, and peripheral vascular disorders. The voltage-dependent Ca2+ channels exist in a number of subclasses characterized by electrophysiologic, permeation, and pharmacologic criteria. The Ca2+ channel antagonists, including verapamil, nifedipine, and diltiazem, serve to characterize th

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2

Greenberg, David A. "Calcium channels and calcium channel antagonists." Annals of Neurology 21, no. 4 (1987): 317–30. http://dx.doi.org/10.1002/ana.410210402.

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3

Collier, M. L., G. Ji, Y. X. Wang, and M. I. Kotlikoff. "Calcium-Induced Calcium Release in Smooth Muscle." Journal of General Physiology 115, no. 5 (2000): 653–62. http://dx.doi.org/10.1085/jgp.115.5.653.

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Calcium-induced calcium release (CICR) has been observed in cardiac myocytes as elementary calcium release events (calcium sparks) associated with the opening of L-type Ca2+ channels. In heart cells, a tight coupling between the gating of single L-type Ca2+ channels and ryanodine receptors (RYRs) underlies calcium release. Here we demonstrate that L-type Ca2+ channels activate RYRs to produce CICR in smooth muscle cells in the form of Ca2+ sparks and propagated Ca2+ waves. However, unlike CICR in cardiac muscle, RYR channel opening is not tightly linked to the gating of L-type Ca2+ channels. L

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4

Mochida, Sumiko. "Presynaptic Calcium Channels." International Journal of Molecular Sciences 20, no. 9 (2019): 2217. http://dx.doi.org/10.3390/ijms20092217.

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Presynaptic Ca2+ entry occurs through voltage-gated Ca2+ (CaV) channels which are activated by membrane depolarization. Depolarization accompanies neuronal firing and elevation of Ca2+ triggers neurotransmitter release from synaptic vesicles. For synchronization of efficient neurotransmitter release, synaptic vesicles are targeted by presynaptic Ca2+ channels forming a large signaling complex in the active zone. The presynaptic CaV2 channel gene family (comprising CaV2.1, CaV2.2, and CaV2.3 isoforms) encode the pore-forming α1 subunit. The cytoplasmic regions are responsible for channel modula

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5

Friedman, P. A., and F. A. Gesek. "Hormone-responsive Ca2+ entry in distal convoluted tubules." Journal of the American Society of Nephrology 4, no. 7 (1994): 1396–404. http://dx.doi.org/10.1681/asn.v471396.

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This editorial review focuses on recent observations regarding the mechanism and regulation of calcium transport in hormone-sensitive distal convoluted tubules. Parathyroid hormone (PTH) and calcitonin increase active calcium absorption by distal convoluted tubules. Occupancy of these peptide hormone receptors results in the activation of both protein kinase A and protein kinase C. The inhibition of either kinase blocks calcium transport. The time course of stimulation of calcium entry in distal convoluted tubules by PTH is slow compared with that by calcitonin. The latency associated with PTH

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6

Reuter, H., S. Kokubun, and B. Prod'hom. "Properties and modulation of cardiac calcium channels." Journal of Experimental Biology 124, no. 1 (1986): 191–201. http://dx.doi.org/10.1242/jeb.124.1.191.

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Voltage-dependent calcium channels are widely distributed in excitable membranes and are involved in the regulation of many cellular functions. These channels can be modulated by neurotransmitters and drugs. There is one particular type of calcium channel in cardiac cells (L-type) whose gating is affected in different ways by beta-adrenoceptor and 1,4-dihydropyridine agonists. We have analysed single calcium channel currents (i) in myocytes from rat hearts in the absence and presence of isoproterenol or 8-bromo-cAMP. We have found that both compounds have similar effects on calcium channel pro

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7

Gollasch, M., J. Hescheler, J. M. Quayle, J. B. Patlak, and M. T. Nelson. "Single calcium channel currents of arterial smooth muscle at physiological calcium concentrations." American Journal of Physiology-Cell Physiology 263, no. 5 (1992): C948—C952. http://dx.doi.org/10.1152/ajpcell.1992.263.5.c948.

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Entry of Ca through voltage-dependent Ca channels is an important regulator of the function of smooth muscle, cardiac muscle, and neurons. Although Ca channels have been extensively studied since the first descriptions of Ca action potentials (P. Fatt and B. Katz. J. Physiol. Lond. 120: 171-204, 1953), the permeation rate of Ca through single Ca channels has not been measured directly under physiological conditions. Instead, single Ca channels have typically been examined using high concentrations (80-110 mM) of another divalent charge carrier, Ba, so as to maximize the amplitude of the single

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8

Shuttleworth, T. J., and O. Mignen. "Calcium entry and the control of calcium oscillations." Biochemical Society Transactions 31, no. 5 (2003): 916–19. http://dx.doi.org/10.1042/bst0310916.

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During oscillatory Ca2+ signals, the agonist-induced enhanced entry of extracellular Ca2+ plays a critical role in modulating the frequency of the oscillations. Although it was originally assumed that the entry of Ca2+ under these conditions occurred via the well-known, and apparently ubiquitous, store-operated mechanism, subsequent studies suggested that this was unlikely. It is now known that, in many cell types, a novel non-capacitative Ca2+-selective pathway whose activation is dependent on arachidonic acid is responsible, and the channels involved [ARC channels (arachidonate-regulated Ca2

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9

Triggle, C. R., and M. Wolowyk. "Calcium Channels Symposium." Canadian Journal of Physiology and Pharmacology 68, no. 11 (1990): 1472–73. http://dx.doi.org/10.1139/y90-223.

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Calcium is an essential element for just about all cellular processes, and yet abnormally high levels of cellular calcium can cause cell death. The processes that control cellular levels of this metal ion are thus of critical importance to both normal and pathophysiological conditions. Essential in the regulation of intracellular calcium levels are the calcium channels associated with cell membranes, for instance, with the plasma and sarcoplasmic reticulum membranes of muscle cells. In recent years, there has been a tremendous increase in our knowledge of the structure and function of these ch

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10

Kolesnikov, D. O., E. R. Grigorieva, M. A. Nomerovskaya, D. S. Reshetin, A. V. Shalygin, and E. V. Kaznacheyeva. "The Effect of Calcium Ions on the Electrophysiological Properties of Single ANO6 Channels." Acta Naturae 16, no. 1 (2024): 40–47. http://dx.doi.org/10.32607/actanaturae.27338.

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Proteins belonging to the anoctamin (ANO) family form calcium-activated chloride channels (CaCCs). The most unusual member of this family, ANO6 (TMEM16F), simultaneously exhibits the functions of calcium-dependent scramblase and the ion channel. ANO6 affects the plasma membrane dynamics and phosphatidylserine transport; it is also involved in programmed cell death. The properties of ANO6 channels remain the subject of debate. In this study, we investigated the effect of variations in the intracellular and extracellular concentrations of calcium ions on the electrophysiological properties of en

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11

BIEDA, MARK C., and DAVID R. COPENHAGEN. "N-type and L-type calcium channels mediate glycinergic synaptic inputs to retinal ganglion cells of tiger salamanders." Visual Neuroscience 21, no. 4 (2004): 545–50. http://dx.doi.org/10.1017/s0952523804214055.

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Synaptically localized calcium channels shape the timecourse of synaptic release, are a prominent site for neuromodulation, and have been implicated in genetic disease. In retina, it is well established that L-type calcium channels play a major role in mediating release of glutamate from the photoreceptors and bipolar cells. However, little is known about which calcium channels are coupled to synaptic exocytosis of glycine, which is primarily released by amacrine cells. A recent report indicates that glycine release from spiking AII amacrine cells relies exclusively upon L-type calcium channel

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12

Luo, Fujun, Markus Dittrich, Soyoun Cho, Joel R. Stiles, and Stephen D. Meriney. "Transmitter release is evoked with low probability predominately by calcium flux through single channel openings at the frog neuromuscular junction." Journal of Neurophysiology 113, no. 7 (2015): 2480–89. http://dx.doi.org/10.1152/jn.00879.2014.

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The quantitative relationship between presynaptic calcium influx and transmitter release critically depends on the spatial coupling of presynaptic calcium channels to synaptic vesicles. When there is a close association between calcium channels and synaptic vesicles, the flux through a single open calcium channel may be sufficient to trigger transmitter release. With increasing spatial distance, however, a larger number of open calcium channels might be required to contribute sufficient calcium ions to trigger vesicle fusion. Here we used a combination of pharmacological calcium channel block,

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13

Vasu, Sreerag Othayoth, and Hanoch Kaphzan. "Direct Current Stimulation Modulates Synaptic Facilitation via Distinct Presynaptic Calcium Channels." International Journal of Molecular Sciences 24, no. 23 (2023): 16866. http://dx.doi.org/10.3390/ijms242316866.

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Transcranial direct current stimulation (tDCS) is a subthreshold neurostimulation technique known for ameliorating neuropsychiatric conditions. The principal mechanism of tDCS is the differential polarization of subcellular neuronal compartments, particularly the axon terminals that are sensitive to external electrical fields. Yet, the underlying mechanism of tDCS is not fully clear. Here, we hypothesized that direct current stimulation (DCS)-induced modulation of presynaptic calcium channel conductance alters axon terminal dynamics with regard to synaptic vesicle release. To examine the invol

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14

Manira, A. El, and N. Bussières. "Calcium Channel Subtypes in Lamprey Sensory and Motor Neurons." Journal of Neurophysiology 78, no. 3 (1997): 1334–40. http://dx.doi.org/10.1152/jn.1997.78.3.1334.

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El Manira, A. and N. Bussières. Calcium channel subtypes in lamprey sensory and motor neurons. J. Neurophysiol. 78: 1334–1340, 1997. Pharmacologically distinct calcium channels have been characterized in dissociated cutaneous sensory neurons and motoneurons of the larval lamprey spinal cord. To enable cell identification, sensory dorsal cells and motoneurons were selectively labeled with fluorescein-coupled dextran amine in the intact spinal cord in vitro before dissociation. Calcium channels present in sensory dorsal cells, motoneurons, and other spinal cord neurons were characterized with th

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15

Seagar, Michael, Christian Lévêque, Nathalie Charvin, et al. "Interactions between proteins implicated in exocytosis and voltage–gated calcium channels." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 354, no. 1381 (1999): 289–97. http://dx.doi.org/10.1098/rstb.1999.0380.

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Neurotransmitter release from synaptic vesicles is triggered by voltage–gated calcium influx through P/Q–type or N–type calcium channels. Purification of N–type channels from rat brain synaptosomes initially suggested molecular interactions between calcium channels and two key proteins implicated in exocytosis: synaptotagmin I and syntaxin 1. Co–immunoprecipitation experiments were consistent with the hypothesis that both N– and P/Q–type calcium channels, but not L–type channels, are associated with the 7S complex containing syntaxin 1, SNAP–25, VAMP and synaptotagmin I or II. Immunofluorescen

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16

Rosenberg, R. L., P. Hess, and R. W. Tsien. "Cardiac calcium channels in planar lipid bilayers. L-type channels and calcium-permeable channels open at negative membrane potentials." Journal of General Physiology 92, no. 1 (1988): 27–54. http://dx.doi.org/10.1085/jgp.92.1.27.

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Planar lipid bilayer recordings were used to study Ca channels from bovine cardiac sarcolemmal membranes. Ca channel activity was recorded in the absence of nucleotides or soluble enzymes, over a range of membrane potentials and ionic conditions that cannot be achieved in intact cells. The dihydropyridine-sensitive L-type Ca channel, studied in the presence of Bay K 8644, was identified by a detailed comparison of its properties in artificial membranes and in intact cells. L-type Ca channels in bilayers showed voltage dependence of channel activation and inactivation, open and closed times, an

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17

Mayo, Sonia, Irene Gómez-Manjón, Ana Victoria Marco-Hernández, Francisco Javier Fernández-Martínez, Ana Camacho, and Francisco Martínez. "N-Type Ca Channel in Epileptic Syndromes and Epilepsy: A Systematic Review of Its Genetic Variants." International Journal of Molecular Sciences 24, no. 7 (2023): 6100. http://dx.doi.org/10.3390/ijms24076100.

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N-type voltage-gated calcium channel controls the release of neurotransmitters from neurons. The association of other voltage-gated calcium channels with epilepsy is well-known. The association of N-type voltage-gated calcium channels and pain has also been established. However, the relationship between this type of calcium channel and epilepsy has not been specifically reviewed. Therefore, the present review systematically summarizes existing publications regarding the genetic associations between N-type voltage-dependent calcium channel and epilepsy.

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18

Mangel, A. W., L. Scott, and R. A. Liddle. "Depolarization-stimulated cholecystokinin secretion is mediated by L-type calcium channels in STC-1 cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 2 (1996): G287—G290. http://dx.doi.org/10.1152/ajpgi.1996.270.2.g287.

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To examine the role of calcium channels in depolarization-activated cholecystokinin (CCK) release, studies were performed in an intestinal CCK-secreting cell line, STC-1. Blockade of potassium channels with barium chloride (5 mM) increased the release of CCK by 374.6 +/- 46.6% of control levels. Barium-induced secretion was inhibited by the L-type calcium-channel blocker, nicardipine. Nicardipine (10(-9)-10(-5) M) produced a dose-dependent inhibition in barium-stimulated secretion with a half-maximal inhibition (IC50) value of 0.1 microM. A second L-type calcium-channel blocker, diltiazem (10(

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19

Braun, Andrew P. "Ammonium ion enhances the calcium-dependent gating of a mammalian large conductance, calcium-sensitive K+ channel." Canadian Journal of Physiology and Pharmacology 79, no. 11 (2001): 919–23. http://dx.doi.org/10.1139/y01-076.

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We observed that the current amplitude and activation of expressed, mouse brain large conductance, calcium-sensitive K+ channels (BKCa channels) may be reversibly enhanced following addition of low concentrations of the weakly permeant cation NH4+ to the cytoplasmic face of the channel in excised, inside-out membrane patches from HEK 293 cells. Conductance-voltage relations were left-shifted along the voltage axis by addition of NH4Cl in a concentration-dependent manner, with an EC50 of 18.5 mM. Furthermore, this effect was observed in the presence of cytosolic free calcium (~1 µM), but was ab

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20

Pallotta, B. S. "N-bromoacetamide removes a calcium-dependent component of channel opening from calcium-activated potassium channels in rat skeletal muscle." Journal of General Physiology 86, no. 5 (1985): 601–11. http://dx.doi.org/10.1085/jgp.86.5.601.

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Calcium-activated potassium channels from cultured rat skeletal muscle were treated with the protein-modifying reagent N-bromoacetamide (NBA) (0.3-1 mM) and studied in excised patches using patch-clamp techniques. After NBA treatment, channels opened only occasionally, and, in contrast to untreated channels, the open probability was no longer sensitive to intracellular surface calcium ions (1 nM to 100 microM). Channel activity did, however, exhibit a voltage dependence similar in direction and magnitude to that shown before NBA treatment (increasing e-fold with 19 mV depolarization). Distribu

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21

Davis, Scott F., and Cindy L. Linn. "Mechanism linking NMDA receptor activation to modulation of voltage-gated sodium current in distal retina." American Journal of Physiology-Cell Physiology 284, no. 5 (2003): C1193—C1204. http://dx.doi.org/10.1152/ajpcell.00256.2002.

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In this study, we investigated the mechanism that links activation of N-methyl-D-aspartate (NMDA) receptors to inhibition of voltage-gated sodium channels in isolated catfish cone horizontal cells. NMDA channels were activated in voltage-clamped cells incubated in low-calcium saline or dialyzed with the calcium chelator BAPTA to determine that calcium influx through NMDA channels is required for sodium channel modulation. To determine whether calcium influx through NMDA channels triggers calcium-induced calcium release (CICR), cells were loaded with the calcium-sensitive dye calcium green 2 an

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22

Noyer, Lucile, Loic Lemonnier, Pascal Mariot, and Dimitra Gkika. "Partners in Crime: Towards New Ways of Targeting Calcium Channels." International Journal of Molecular Sciences 20, no. 24 (2019): 6344. http://dx.doi.org/10.3390/ijms20246344.

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The characterization of calcium channel interactome in the last decades opened a new way of perceiving ion channel function and regulation. Partner proteins of ion channels can now be considered as major components of the calcium homeostatic mechanisms, while the reinforcement or disruption of their interaction with the channel units now represents an attractive target in research and therapeutics. In this review we will focus on the targeting of calcium channel partner proteins in order to act on the channel activity, and on its consequences for cell and organism physiology. Given the recent

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23

Pozdnyakov, Ilya, Olga Matantseva, and Sergei Skarlato. "Consensus channelome of dinoflagellates revealed by transcriptomic analysis sheds light on their physiology." Algae 36, no. 4 (2021): 315–26. http://dx.doi.org/10.4490/algae.2021.36.12.2.

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Ion channels are membrane protein complexes mediating passive ion flux across the cell membranes. Every organism has a certain set of ion channels that define its physiology. Dinoflagellates are ecologically important microorganisms characterized by effective physiological adaptability, which backs up their massive proliferations that often result in harmful blooms (red tides). In this study, we used a bioinformatics approach to identify homologs of known ion channels that belong to 36 ion channel families. We demonstrated that the versatility of the dinoflagellate physiology is underpinned by

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24

Bennett, Brian D., Ulises Alvarez, and Keith A. Hruska. "Receptor-Operated Osteoclast Calcium Sensing*." Endocrinology 142, no. 5 (2001): 1968–74. http://dx.doi.org/10.1210/endo.142.5.8125.

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Abstract Osteoclasts “sense” elevated extracellular calcium, which leads to cytoskeletal changes that may be linked to phospholipase C (PLC) activation and the associated rise in intracellular calcium ([Ca2+]i). Since PLC is linked to transient receptor potential channels (trp), we hypothesized that receptor activated calcium influx due to this channel type would be activated by osteoclasts sensing [Ca2+]e. We found that high [Ca2+]e induced similar intracellular Ca2+ rises in chicken osteoclasts with or without intracellular Ca2+ store depletion by either TPEN or thapsigargin, thus defining s

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25

Glossmann, H., D. R. Ferry, A. Goll, J. Striessnig, and M. Schober. "Calcium Channels." Journal of Cardiovascular Pharmacology 7 (1985): S20—S30. http://dx.doi.org/10.1097/00005344-198500076-00005.

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26

Rodger, Ian W. "Calcium Channels." American Review of Respiratory Disease 136, no. 4_pt_2 (1987): S15—S17. http://dx.doi.org/10.1164/ajrccm/136.4_pt_2.s15.

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27

PETERSEN, O. H. "Calcium channels." Nature 336, no. 6199 (1988): 528. http://dx.doi.org/10.1038/336528a0.

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28

Yu, Alan S. L. "Calcium channels." Current Opinion in Nephrology and Hypertension 3, no. 5 (1994): 497–503. http://dx.doi.org/10.1097/00041552-199409000-00004.

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29

Schwartz, Arnold. "Calcium channels." Journal of Molecular and Cellular Cardiology 24 (May 1992): 33. http://dx.doi.org/10.1016/0022-2828(92)90130-r.

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30

Estacion, M., H. B. Nguyen, and J. J. Gargus. "Calcium is permeable through a maitotoxin-activated nonselective cation channel in mouse L cells." American Journal of Physiology-Cell Physiology 270, no. 4 (1996): C1145—C1152. http://dx.doi.org/10.1152/ajpcell.1996.270.4.c1145.

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The shellfish poison maitotoxin causes the irreversible opening of nonselective cation channels in mouse L cell fibroblasts, consistent with the action of this toxin in other cell types and the previously demonstrated existence of 28-pS voltage-insensitive nonselected cation channels that are activated by platelet-derived growth factor in these cells. Toxin-induced opening of these nonselective cation channels led to increases of intracellular calcium and secondary activation of calcium-activated potassium channel. These effects were completely dependent on influx of extracellular calcium, sup

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31

McCleskey, E. W., A. P. Fox, D. Feldman, and R. W. Tsien. "Different types of calcium channels." Journal of Experimental Biology 124, no. 1 (1986): 177–90. http://dx.doi.org/10.1242/jeb.124.1.177.

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Ca2+ channels allow passage of Ca2+ ions into the cytoplasm through a selective pore which is opened in response to depolarization of the cell membrane (for reviews see Hagiwara & Byerly, 1981, 1983; Tsien, 1983; Reuter, 1983). The Ca2+ flux creates a net inward, depolarizing current and the resulting accumulation of Ca2+ in the cytoplasm can act as a chemical trigger for secretion of hormones and neurotransmitters, contraction of muscle and a variety of other Ca2+-sensitive events. Thus, upon sensing membrane potential changes, Ca2+ channels simultaneously generate an electrical signal wh

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32

Fill, Michael, and Julio A. Copello. "Ryanodine Receptor Calcium Release Channels." Physiological Reviews 82, no. 4 (2002): 893–922. http://dx.doi.org/10.1152/physrev.00013.2002.

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The ryanodine receptors (RyRs) are a family of Ca2+ release channels found on intracellular Ca2+ storage/release organelles. The RyR channels are ubiquitously expressed in many types of cells and participate in a variety of important Ca2+ signaling phenomena (neurotransmission, secretion, etc.). In striated muscle, the RyR channels represent the primary pathway for Ca2+ release during the excitation-contraction coupling process. In general, the signals that activate the RyR channels are known (e.g., sarcolemmal Ca2+ influx or depolarization), but the specific mechanisms involved are still bein

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Mendelowitz, D., P. J. Reynolds, and M. C. Andresen. "Heterogeneous functional expression of calcium channels at sensory and synaptic regions in nodose neurons." Journal of Neurophysiology 73, no. 2 (1995): 872–75. http://dx.doi.org/10.1152/jn.1995.73.2.872.

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1. In the present study we have taken advantage of the unique anatomy of visceral sensory neurons that enabled us to isolate and examine the role of calcium channel subtypes at the soma, central synaptic terminals, and peripheral sensory endings. 2. N-type calcium channels dominated somatic currents (60%), with lesser (16% and 12%) contributions from P- and L-type channels, respectively, in patch-clamped dispersed nodose neurons using toxins selective for each calcium channel subtype. 3. These toxins also blocked the release of neurotransmitters from these visceral synaptic terminals in a brai

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Hyde, James, Nebojsa Kezunovic, Francisco J. Urbano, and Edgar Garcia-Rill. "Spatiotemporal properties of high-speed calcium oscillations in the pedunculopontine nucleus." Journal of Applied Physiology 115, no. 9 (2013): 1402–14. http://dx.doi.org/10.1152/japplphysiol.00762.2013.

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The pedunculopontine nucleus (PPN) is a component of the reticular activating system (RAS), and is involved in the activated states of waking and rapid eye movement (REM) sleep. Gamma oscillations (approximately 30–80 Hz) are evident in all PPN neurons and are mediated by high-threshold voltage-dependent N- and P/Q-type calcium channels. We tested the hypothesis that high-speed calcium imaging would reveal calcium-mediated oscillations in dendritic compartments in synchrony with patch-clamp recorded oscillations during depolarizing current ramps. Patch-clamped 8- to 16-day-old rat PPN neurons

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Taylor, James T., Luping Huang, Brian M. Keyser, Hean Zhuang, Craig W. Clarkson та Ming Li. "Role of high-voltage-activated calcium channels in glucose-regulated β-cell calcium homeostasis and insulin release". American Journal of Physiology-Endocrinology and Metabolism 289, № 5 (2005): E900—E908. http://dx.doi.org/10.1152/ajpendo.00101.2005.

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High-voltage-activated (HVA) calcium channels are known to be the primary source of calcium for glucose-stimulated insulin secretion. However, few studies have investigated how these channels can be regulated by chronically elevated levels of glucose. In the present study, we determined the level of expression of the four major HVA calcium channels (N-type, P/Q-type, LC-type, and LD-type) in rat pancreatic β-cells. Using quantitative real-time PCR (QRT-PCR), we found the expression of all four HVA genes in rat insulinoma cells (INS-1) and in primary isolated rat islet cells. We then determined

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Dolphin, Annette C. "Voltage-gated calcium channels: Their discovery, function and importance as drug targets." Brain and Neuroscience Advances 2 (January 2018): 239821281879480. http://dx.doi.org/10.1177/2398212818794805.

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This review will first describe the importance of Ca2+ entry for function of excitable cells, and the subsequent discovery of voltage-activated calcium conductances in these cells. This finding was rapidly followed by the identification of multiple subtypes of calcium conductance in different tissues. These were initially termed low- and high-voltage activated currents, but were then further subdivided into L-, N-, PQ-, R- and T-type calcium currents on the basis of differing pharmacology, voltage-dependent and kinetic properties, and single channel conductance. Purification of skeletal muscle

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Isaev, Dmytro, Karisa Solt, Oksana Gurtovaya, John P. Reeves, and Roman Shirokov. "Modulation of the Voltage Sensor of L-type Ca2+ Channels by Intracellular Ca2+." Journal of General Physiology 123, no. 5 (2004): 555–71. http://dx.doi.org/10.1085/jgp.200308876.

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Both intracellular calcium and transmembrane voltage cause inactivation, or spontaneous closure, of L-type (CaV1.2) calcium channels. Here we show that long-lasting elevations of intracellular calcium to the concentrations that are expected to be near an open channel (≥100 μM) completely and reversibly blocked calcium current through L-type channels. Although charge movements associated with the opening (ON) motion of the channel's voltage sensor were not altered by high calcium, the closing (OFF) transition was impeded. In two-pulse experiments, the blockade of calcium current and the reducti

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Putney, James W. "Capacitative calcium entry." Journal of Cell Biology 169, no. 3 (2005): 381–82. http://dx.doi.org/10.1083/jcb.200503161.

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A long-standing mystery in the cell biology of calcium channel regulation is the nature of the signal linking intracellular calcium stores to plasma membrane capacitative calcium entry channels. An RNAi-based screen of selected Drosophila genes has revealed that a calcium-binding protein, stromal interaction molecule (STIM), plays an essential role in the activation of these channels and may be the long sought sensor of calcium store content.

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Yang, Tingting, Min He, Hailiang Zhang, Paula Q. Barrett, and Changlong Hu. "L- and T-type calcium channels control aldosterone production from human adrenals." Journal of Endocrinology 244, no. 1 (2020): 237–47. http://dx.doi.org/10.1530/joe-19-0259.

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Aldosterone, which plays a key role in the regulation of blood pressure, is produced by zona glomerulosa (ZG) cells of the adrenal cortex. Exaggerated overproduction of aldosterone from ZG cells causes primary hyperaldosteronism. In ZG cells, calcium entry through voltage-gated calcium channels plays a central role in the regulation of aldosterone secretion. Previous studies in animal adrenals and human adrenal adrenocortical cell lines suggest that the T-type but not the L-type calcium channel activity drives aldosterone production. However, recent clinical studies show that somatic mutations

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Chen, Nanjun, and Qigeng Fang. "Review the Regulation of Plasma Membrane Calcium Channel in Cancer and Patch Clamp Technique." E3S Web of Conferences 271 (2021): 04037. http://dx.doi.org/10.1051/e3sconf/202127104037.

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As one of the most versatile and universal second messengers, calcium plays an essential role in cell life. Here we briefly reviewed the research progress of how different calcium channels are located at the cell plasma membrane, including voltage-gated calcium channels (VGCCs), receptor-operated channels (ROC), and store-operated channels (ROC). These channels can regulate different cancer progression. Afterward, the patch clamp technique's development and operating principle, an important quantitative method used for ion channel investigation, are introduced in this paper.

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Yan, Jiusheng, Qin Li, and Richard W. Aldrich. "Closed state-coupled C-type inactivation in BK channels." Proceedings of the National Academy of Sciences 113, no. 25 (2016): 6991–96. http://dx.doi.org/10.1073/pnas.1607584113.

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Ion channels regulate ion flow by opening and closing their pore gates. K+ channels commonly possess two pore gates, one at the intracellular end for fast channel activation/deactivation and the other at the selectivity filter for slow C-type inactivation/recovery. The large-conductance calcium-activated potassium (BK) channel lacks a classic intracellular bundle-crossing activation gate and normally show no C-type inactivation. We hypothesized that the BK channel’s activation gate may spatially overlap or coexist with the C-type inactivation gate at or near the selectivity filter. We induced

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Chen, Xinzhe. "Research progress on calcium-activated potassium ion channels." Theoretical and Natural Science 62, no. 1 (2024): 160–65. http://dx.doi.org/10.54254/2753-8818/62/20241522.

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Abstract. Potassium ion channels are diverse and widely distributed, playing a key role in a variety of physiological and pathological processes. According to the size of the conductance, they can be divided into large conductive calcium activated potassium channel (BK channel), medium conductive calcium activated potassium channel (IK channel) and small conductive calcium activated potassium channel (SK channel). In recent years, remarkable progress has been made in studying these three ion channels, and a series of therapeutic drugs have emerged. According to the single channel conductance,

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Yarotskyy, Viktor, Guofeng Gao, Blaise Z. Peterson, and Keith S. Elmslie. "Domain III regulates N-type (CaV2.2) calcium channel closing kinetics." Journal of Neurophysiology 107, no. 7 (2012): 1942–51. http://dx.doi.org/10.1152/jn.00993.2011.

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CaV2.2 (N-type) and CaV1.2 (L-type) calcium channels gate differently in response to membrane depolarization, which is critical to the unique physiological functions mediated by these channels. We wondered if the source for these differences could be identified. As a first step, we examined the effect of domain exchange between N-type and L-type channels on activation-deactivation kinetics, which were significantly different between these channels. Kinetic analysis of chimeric channels revealed N-channel-like deactivation for all chimeric channels containing N-channel domain III, while activat

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Wang, Dan, Lotten Ragnarsson, and Richard J. Lewis. "T-type Calcium Channels in Health and Disease." Current Medicinal Chemistry 27, no. 19 (2020): 3098–122. http://dx.doi.org/10.2174/0929867325666181001112821.

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Low Voltage-Activated (LVA) T-type calcium channels are characterized by transient current and Low Threshold Spikes (LTS) that trigger neuronal firing and oscillatory behavior. Combined with their preferential localization in dendrites and their specific “window current”, T-type calcium channels are considered to be key players in signal amplification and synaptic integration. Assisted by the emerging pharmacological tools, the structural determinants of channel gating and kinetics, as well as novel physiological and pathological functions of T-type calcium channels, are being uncovered. In th

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Shah, Kajol, Sarah Seeley, Castin Schulz, Jacqueline Fisher, and Shubha Gururaja Rao. "Calcium Channels in the Heart: Disease States and Drugs." Cells 11, no. 6 (2022): 943. http://dx.doi.org/10.3390/cells11060943.

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Calcium ions are the major signaling ions in the cells. They regulate muscle contraction, neurotransmitter secretion, cell growth and migration, and the activity of several proteins including enzymes and ion channels and transporters. They participate in various signal transduction pathways, thereby regulating major physiological functions. Calcium ion entry into the cells is regulated by specific calcium channels and transporters. There are mainly six types of calcium channels, of which only two are prominent in the heart. In cardiac tissues, the two types of calcium channels are the L type a

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Wang, Jijiang, Mustapha Irnaten, and David Mendelowitz. "Agatoxin-IVA-Sensitive Calcium Channels Mediate the Presynaptic and Postsynaptic Nicotinic Activation of Cardiac Vagal Neurons." Journal of Neurophysiology 85, no. 1 (2001): 164–68. http://dx.doi.org/10.1152/jn.2001.85.1.164.

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Whole cell currents and miniature glutamatergic synaptic events (minis) were recorded in vitro from cardiac vagal neurons in the nucleus ambiguus using the patch-clamp technique. We examined whether voltage-dependent calcium channels were involved in the nicotinic excitation of cardiac vagal neurons. Nicotine evoked an inward current, increase in mini amplitude, and increase in mini frequency in cardiac vagal neurons. These responses were inhibited by the nonselective voltage-dependent calcium channel blocker Cd (100 μM). The P-type voltage-dependent calcium channel blocker agatoxin IVA (100 n

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Büschges, A., M. A. Wikström, S. Grillner, and A. El Manira. "Roles of High-Voltage–Activated Calcium Channel Subtypes in a Vertebrate Spinal Locomotor Network." Journal of Neurophysiology 84, no. 6 (2000): 2758–66. http://dx.doi.org/10.1152/jn.2000.84.6.2758.

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Lamprey spinal cord neurons possess N-, L-, and P/Q-type high-voltage–activated (HVA) calcium channels. We have analyzed the role of the different HVA calcium channels subtypes in the overall functioning of the spinal locomotor network by monitoring the influence of their specific agonists and antagonists on synaptic transmission and on N-methyl-d-aspartate (NMDA)–elicited fictive locomotion. The N-type calcium channel blocker ω-conotoxin GVIA (ω-CgTx) depressed synaptic transmission from excitatory and inhibitory interneurons. Blocking L-type and P/Q-type calcium channels with nimodipine and

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Syamsunarno, Mas Rizky Anggun Adipurna, Alif Bagus Rakhimullah, Uni Gamayani, et al. "Iron Administration Affects Cardiac Calcium Channel Expression in Mice: The Role of Cardiac Calcium Channel Expression in The Heart of Iron Overload Mice Model." Indonesian Biomedical Journal 12, no. 3 (2020): 261–6. http://dx.doi.org/10.18585/inabj.v12i3.1170.

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BACKGROUND: Iron-overload cardiomyopathy (IOC) is a major comorbidity in patients with chronic repetitive blood transfusion due to myocardial iron uptake that facilitated by calcium channels. As cardiac compensatory mechanism to IOC, we hypothesized the cardiac calcium channels expression would be increased and involved in cardiomyopathy progressivity. This study was aimed to investigate the gene expression of calcium channels in the heart of the iron overload mice model.METHODS: Mice were divided into three groups according to iron administration doses 0, 0.1, and 0.3 mg/day. Systolic blood p

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Nunoki, K., V. Florio, and W. A. Catterall. "Activation of purified calcium channels by stoichiometric protein phosphorylation." Proceedings of the National Academy of Sciences 86, no. 17 (1989): 6816–20. http://dx.doi.org/10.1073/pnas.86.17.6816.

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Purified dihydropyridine-sensitive calcium channels from rabbit skeletal muscle were reconstituted into phosphatidylcholine vesicles to evaluate the effect of phosphorylation by cyclic AMP-dependent protein kinase (PK-A) on their function. Both the rate and extent of 45Ca2+ uptake into vesicles containing reconstituted calcium channels were increased severalfold after incubation with ATP and PK-A. The degree of stimulation of 45Ca2+ uptake was linearly proportional to the extent of phosphorylation of the alpha 1 and beta subunits of the calcium channel up to a stoichiometry of approximately 1

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Chen, Xingjuan, Ruiyuan Cao, and Wu Zhong. "Host Calcium Channels and Pumps in Viral Infections." Cells 9, no. 1 (2019): 94. http://dx.doi.org/10.3390/cells9010094.

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Ca2+ is essential for virus entry, viral gene replication, virion maturation, and release. The alteration of host cells Ca2+ homeostasis is one of the strategies that viruses use to modulate host cells signal transduction mechanisms in their favor. Host calcium-permeable channels and pumps (including voltage-gated calcium channels, store-operated channels, receptor-operated channels, transient receptor potential ion channels, and Ca2+-ATPase) mediate Ca2+ across the plasma membrane or subcellular organelles, modulating intracellular free Ca2+. Therefore, these Ca2+ channels or pumps present im

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