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Добірка наукової літератури з теми "L-typa calcium channels"

Автор: Grafiati

Опубліковано: 11 березня 2023

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Статті в журналах з теми "L-typa calcium channels"

1

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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2

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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3

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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4

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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5

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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6

Liu, Xiaoyu, Tingting Yang, Langxi Miao, Yan-Ai Mei, and Changlong Hu. "Leukotriene B4 Inhibits L-Type Calcium Channels via p38 Signaling Pathway in Vascular Smooth Muscle Cells." Cellular Physiology and Biochemistry 37, no. 5 (2015): 1903–13. http://dx.doi.org/10.1159/000438551.

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Background/Aims: Arachidonic acid (AA) and its metabolites are important endogenous lipid messengers. In this study, we test the effect of Leukotriene B4 (LTB4), a 5-lipoxygenase metabolite of AA, on L-type calcium channels in A7r5 rat aortic vascular smooth muscle cells. Methods: L-type calcium channel currents were recorded by a patch-clamp technique. The mRNA expression of CaV1.2 was determined by Real-time RT-PCR. The protein expression of CaV1.2 and p38 activity was determined by Western blot analysis. Results: LTB4 inhibits L-type channel currents in A7r5 cells in a dose-and time- depend

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7

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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8

Durante, P., C. G. Cardenas, J. A. Whittaker, S. T. Kitai, and R. S. Scroggs. "Low-Threshold L-type Calcium Channels in Rat Dopamine Neurons." Journal of Neurophysiology 91, no. 3 (2004): 1450–54. http://dx.doi.org/10.1152/jn.01015.2003.

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Ca2+ channel subtypes expressed by dopaminergic (DA) neurons in the substantia nigra pars compacta (SNc) were studied using whole cell patch-clamp recordings and blockers selective for different channel types (L, N, and P/Q). Nimodipine (Nim, 2 μM), ω-conotoxin GVIA (Ctx, 1 μM), or ω-agatoxin IVA (Atx, 50 nM) blocked 27, 36, and 37% of peak whole cell Ca2+ channel current, respectively, indicating the presence of L-, N-, and P-type channels. Nim blocked approximately twice as much Ca2+ channel current near activation threshold compared with Ctx or Atx, suggesting that small depolarizations pre

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9

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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10

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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