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L-type of voltage-gated Ca2+ channel

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https://www.readbyqxmd.com/read/29789806/different-membrane-pathways-mediate-ca-2-influx-in-adrenal-chromaffin-cells-exposed-to-150-400-ns-electric-pulses
#1
Tarique R Bagalkot, Robert C Terhune, Normand Leblanc, Gale L Craviso
Exposing adrenal chromaffin cells to 5 ns electric pulses (nsPEF) causes a rapid rise in intracellular Ca2+ ([Ca2+ ]i ) that is solely the result of Ca2+ influx through voltage-gated Ca2+ channels (VGCCs). This study explored the effect of longer duration nsPEF on [Ca2+ ]i . Single 150, 200, or 400 ns pulses at 3.1 kV/cm evoked rapid increases in [Ca2+ ]i , the magnitude of which increased linearly with pulse width and electric field amplitude. Recovery of [Ca2+ ]i to prestimulus levels was faster for 150 ns exposures...
2018: BioMed Research International
https://www.readbyqxmd.com/read/29789373/voltage-gated-calcium-influx-modifies-cholinergic-inhibition-of-inner-hair-cells-in-the-immature-rat-cochlea
#2
Stephen Zachary, Nathaniel Nowak, Pankhuri Vyas, Luke Bonanni, Paul Albert Fuchs
Until postnatal day 12, inner hair cells of the rat cochlea are invested with both afferent and efferent synaptic connections. With the onset of hearing at P12, the efferent synapses disappear, and afferent (ribbon) synapses operate with greater efficiency. This change coincides with increased expression of voltage-gated potassium channels, the loss of calcium-dependent electrogenesis, and the onset of graded receptor potentials driven by sound. The transient efferent synapses include near-membrane postsynaptic cisterns thought to regulate calcium influx through the hair cell's α9α10-nAChR that activates small conductance Ca2+ -activated K+ (SK) channels...
May 22, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29773754/a-critical-neurodevelopmental-role-for-l-type-voltage-gated-calcium-channels-in-neurite-extension-and-radial-migration
#3
Satoshi Kamijo, Yuichiro Ishii, Shin-Ichiro Horigane, Kanzo Suzuki, Masamichi Ohkura, Junichi Nakai, Hajime Fujii, Sayaka Takemoto-Kimura, Haruhiko Bito
In spite of many association studies linking gene polymorphisms and mutations of L-type Voltage-Gated Ca2+ Channels (VGCC) in neurodevelopmental disorders, such as autism and schizophrenia, specific L-type VGCC roles during brain development remain unclear. Yet, calcium signaling has been shown to be essential for neurodevelopmental processes such as sculpting of neurites, functional wiring and fine tuning of growing networks. To bridge this gap, we performed submembraneous calcium imaging using a membrane-tethered genetically-encoded calcium indicator (GECI) Lck-G-CaMP7...
May 17, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29748133/retinoic-acid-inhibits-neuronal-voltage-gated-calcium-channels
#4
Eric de Hoog, Mark K Lukewich, Gaynor E Spencer
Retinoic acid is the active metabolite of vitamin A and regulates several important cellular processes by activating retinoic acid receptors (RAR) and retinoid X receptors (RXR). These receptors generally act as transcription factors, though non-genomic actions of both retinoic acid and the receptors have also been reported. One such nongenomic effect includes the modulation of Ca2+ levels during homeostatic synaptic plasticity in the hippocampus. Retinoic acid can thus affect Ca2+ signaling and can potentially control both synaptic plasticity and neuronal firing...
February 13, 2018: Cell Calcium
https://www.readbyqxmd.com/read/29742403/alternative-splicing-at-n-terminus-and-domain-i-modulates-ca-v-1-2-inactivation-and-surface-expression
#5
Peter Bartels, Dejie Yu, Hua Huang, Zhenyu Hu, Stefan Herzig, Tuck Wah Soong
The CaV 1.2 L-type calcium channel is a key conduit for Ca2+ influx to initiate excitation-contraction coupling for contraction of the heart and vasoconstriction of the arteries and for altering membrane excitability in neurons. Its α1C pore-forming subunit is known to undergo extensive alternative splicing to produce many CaV 1.2 isoforms that differ in their electrophysiological and pharmacological properties. Here, we examined the structure-function relationship of human CaV 1.2 with respect to the inclusion or exclusion of mutually exclusive exons of the N-terminus exons 1/1a and IS6 segment exons 8/8a...
May 8, 2018: Biophysical Journal
https://www.readbyqxmd.com/read/29738885/regulation-of-seizure-induced-mecp2-ser421-phosphorylation-in-the-developing-brain
#6
Evan C Rosenberg, Jocelyn J Lippman-Bell, Marcus Handy, Samantha S Soldan, Sanjay Rakhade, Cristina Hilario-Gomez, Kaitlyn Folweiler, Leah Jacobs, Frances E Jensen
Neonatal seizures disrupt normal synaptic maturation and often lead to later-life epilepsy and cognitive deficits. During early life, the brain exhibits heightened synaptic plasticity, in part due to a developmental overabundance of CaV 1.2 L-type voltage gated calcium (Ca2+ ) channels (LT-VGCCs) and Ca2+ -permeable AMPARs (CP-AMPARs) lacking GluA2 subunits. We hypothesized that early-life seizures overactivate these channels, in turn dysregulating Ca2+ -dependent signaling pathways including that of methyl-CPG-binding protein 2 (MeCP2), a transcription factor implicated in the autism spectrum disorder (ASD) Rett Syndrome...
May 5, 2018: Neurobiology of Disease
https://www.readbyqxmd.com/read/29694371/voltage-dependent-inward-currents-in-smooth-muscle-cells-of-skeletal-muscle-arterioles
#7
Alexandra V Ulyanova, Roman E Shirokov
Voltage-dependent inward currents responsible for the depolarizing phase of action potentials were characterized in smooth muscle cells of 4th order arterioles in mouse skeletal muscle. Currents through L-type Ca2+ channels were expected to be dominant; however, action potentials were not eliminated in nominally Ca2+-free bathing solution or by addition of L-type Ca2+ channel blocker nifedipine (10 μM). Instead, Na+ channel blocker tetrodotoxin (TTX, 1 μM) reduced the maximal velocity of the upstroke at low, but not at normal (2 mM), Ca2+ in the bath...
2018: PloS One
https://www.readbyqxmd.com/read/29621409/dstac-is-required-for-normal-circadian-activity-rhythms-in-drosophila
#8
I-Uen Hsu, Jeremy W Linsley, Jade E Varineau, Orie T Shafer, John Y Kuwada
The genetic, molecular and neuronal mechanism underlying circadian activity rhythms is well characterized in the brain of Drosophila. The small ventrolateral neurons (s-LNV s) and pigment dispersing factor (PDF) expressed by them are especially important for regulating circadian locomotion. Here we describe a novel gene, Dstac, which is similar to the stac genes found in vertebrates that encode adaptor proteins, which bind and regulate L-type voltage-gated Ca2+ channels (CaChs). We show that Dstac is coexpressed with PDF by the s-LNV s and regulates circadian activity...
April 5, 2018: Chronobiology International
https://www.readbyqxmd.com/read/29617054/activation-of-voltage-gated-sodium-current-and-inhibition-of-erg-mediated-potassium-current-caused-by-telmisartan-an-antagonist-of-angiotensin-ii-type-1-receptor-in-hl-1-atrial-cardiomyocytes
#9
Wei-Ting Chang, Sheng-Nan Wu
Telmisartan (TEL) is a non-peptide blocker of angiotensin II type-1 (AT1 ) receptor. However, the mechanisms through which this drug interacts directly with ion currents in hearts remain largely unclear. Herein, we aim to investigate the effects of TEL the on ionic currents and membrane potential of murine HL-1 cardiomyocytes. In whole-cell recordings, addition of TEL stimulated the peak and late components of voltage-gated Na+ currents (IN a ) with different potencies. The EC50 values required to achieve the stimulatory effect of this drug on peak and late IN a were 0...
April 4, 2018: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/29580153/peripheral-nerve-injury-increases-contribution-of-l-type-calcium-channels-to-synaptic-transmission-in-spinal-lamina-ii-role-of-%C3%AE-2%C3%AE-1-subunits
#10
Sascha Ra Alles, Esperanza Garcia, Sridhar Balasubramanyan, Karen Jones, John R Tyson, Twinkle Joy, Terrance P Snutch, Peter A Smith
Background Following peripheral nerve chronic constriction injury, the accumulation of the α2δ-1 auxiliary subunit of voltage-gated Ca2+ channels in primary afferent terminals contributes to the onset of neuropathic pain. Overexpression of α2δ-1 in Xenopus oocytes increases the opening properties of Cav 1.2 L-type channels and allows Ca2+ influx at physiological membrane potentials. We therefore posited that L-type channels play a role in neurotransmitter release in the superficial dorsal horn in the chronic constriction injury model of neuropathic pain...
January 2018: Molecular Pain
https://www.readbyqxmd.com/read/29548764/cabp1-regulates-ca-v-1-l-type-ca-2-channels-and-their-coupling-to-neurite-growth-and-gene-transcription-in-mouse-spiral-ganglion-neurons
#11
Tian Yang, Ji-Eun Choi, Daniel Soh, Kevin Tobin, Mei-Ling Joiner, Marlan Hansen, Amy Lee
CaBP1 is a Ca2+ binding protein that is widely expressed in neurons in the brain, retina, and cochlea. In heterologous expression systems, CaBP1 interacts with and regulates voltage-gated Cav Ca2+ channels but whether this is the case in neurons is unknown. Here, we investigated the cellular functions of CaBP1 in cochlear spiral ganglion neurons (SGNs), which express high levels of CaBP1. Consistent with the role of CaBP1 as a suppressor of Ca2+ -dependent inactivation (CDI) of Cav 1 (L-type) channels, Cav 1 currents underwent greater CDI in SGNs from mice lacking CaBP1 (C-KO) than in wild-type (WT) SGNs...
April 2018: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/29545262/downregulation-of-l-type-voltage-gated-ca-2-voltage-gated-k-and-large-conductance-ca-2-activated-k-channels-in-vascular-myocytes-from-salt-loading-offspring-rats-exposed-to-prenatal-hypoxia
#12
Bailin Liu, Ruixiu Shi, Xiang Li, Yanping Liu, Xueqin Feng, Xueyi Chen, Xiaorong Fan, Yingying Zhang, Wenna Zhang, Jiaqi Tang, Xiuwen Zhou, Na Li, Xiyuan Lu, Zhice Xu
BACKGROUND: Prenatal hypoxia is suggested to be associated with increased risks of hypertension in offspring. This study tested whether prenatal hypoxia resulted in salt-sensitive offspring and its related mechanisms of vascular ion channel remodeling. METHODS AND RESULTS: Pregnant rats were housed in a normoxic (21% O2 ) or hypoxic (10.5% O2 ) chamber from gestation days 5 to 21. A subset of male offspring received a high-salt diet (8% NaCl) from 4 to 12 weeks after birth...
March 15, 2018: Journal of the American Heart Association
https://www.readbyqxmd.com/read/29522856/effects-of-platelet-activating-factor-on-brain-microvascular-endothelial-cells
#13
Eugen Brailoiu, Christine L Barlow, Servio H Ramirez, Mary E Abood, G Cristina Brailoiu
Platelet-activating factor (PAF) is a potent phospholipid mediator that exerts various pathophysiological effects by interacting with a G protein-coupled receptor. PAF has been reported to increase the permeability of the blood-brain barrier (BBB) via incompletely characterized mechanisms. We investigated the effect of PAF on rat brain microvascular endothelial cells (RBMVEC), a critical component of the BBB. PAF produced a dose-dependent increase in cytosolic Ca2+ concentration; the effect was prevented by the PAF receptor antagonist, WEB2086...
May 1, 2018: Neuroscience
https://www.readbyqxmd.com/read/29522129/neural-cell-adhesion-molecule-2-ncam2-induced-c-src-dependent-propagation-of-submembrane-ca2-spikes-along-dendrites-inhibits-synapse-maturation
#14
Lifu Sheng, Iryna Leshchyns'ka, Vladimir Sytnyk
The neural cell adhesion molecule 2 (NCAM2) is encoded by a gene on chromosome 21 in humans. NCAM2 accumulates in synapses, but its role in regulation of synapse formation remains poorly understood. We demonstrate that an increase in NCAM2 levels results in increased instability of dendritic protrusions and reduced conversion of protrusions to dendritic spines in mouse cortical neurons. NCAM2 overexpression induces an increase in the frequency of submembrane Ca2+ spikes localized in individual dendritic protrusions and promotes propagation of submembrane Ca2+ spikes over segments of dendrites or the whole dendritic tree...
March 7, 2018: Cerebral Cortex
https://www.readbyqxmd.com/read/29477572/multiple-regulatory-actions-of-2-guanidine-4-methylquinazoline-gmq-an-agonist-of-acid-sensing-ion-channel-type-3-on-ionic-currents-in-pituitary-gh-3-cells-and-in-olfactory-sensory-rolf-b1-t-neurons
#15
Edmund Cheung So, Yingwei Wang, Li Qun Yang, Kenny Hsu So, Yi-Ching Lo, Sheng-Nan Wu
GMQ (2-guanidine-4-methylquinazoline or N-(4-methyl-2-quinazolinyl)-guanidine hydrochloride), an agonist of acid-sensing ion channel type 3, has been increasingly used for in vivo studies of alternations in nociceptic behavior. In this study, we tried to investigate whether GMQ has any possible effect on other types of ion channels. Addition of GMQ to pituitary GH3 cells raised the amplitude of Ca2+ -activated K+ currents (IK(Ca) ), which was reversed by verruculogen or PF1022A, but not by TRAM-39. Under inside-out current recordings, addition of GMQ into bath enhanced the probability of large-conductance Ca2+ -activated K+ (BKCa ) channels with an EC50 value of 0...
May 2018: Biochemical Pharmacology
https://www.readbyqxmd.com/read/29473171/nimodipine-confers-clinical-improvement-in-two-models-of-experimental-autoimmune-encephalomyelitis
#16
Jens Ingwersen, Lorenzo De Santi, Britta Wingerath, Jonas Graf, Barbara Koop, Reiner Schneider, Christina Hecker, Friederike Schröter, Mary Bayer, Anna Dorothee Engelke, Michael Dietrich, Philipp Albrecht, Hans-Peter Hartung, Pasquale Annunziata, Orhan Aktas, Tim Prozorovski
Multiple sclerosis (MS) is characterized by inflammatory neurodegeneration, with axonal injury and neuronal cell death occurring in parallel to demyelination. Regarding the molecular mechanisms responsible for demyelination and axonopathy, energy failure, aberrant expression of ion channels and excitotoxicity have been suggested to lead to Ca2+ overload and subsequent activation of calcium-dependent damage pathways. Thus, the inhibition of Ca2+ influx by pharmacological modulation of Ca2+ channels may represent a novel neuroprotective strategy in the treatment of secondary axonopathy...
February 23, 2018: Journal of Neurochemistry
https://www.readbyqxmd.com/read/29431102/pediatric-dilated-cardiomyopathy-associated-lrrc10-leucine-rich-repeat-containing-10-variant-reveals-lrrc10-as-an-auxiliary-subunit-of-cardiac-l-type-ca-2-channels
#17
Marites T Woon, Pamela A Long, Louise Reilly, Jared M Evans, Alexis M Keefe, Martin R Lea, Carl J Beglinger, Ravi C Balijepalli, Youngsook Lee, Timothy M Olson, Timothy J Kamp
BACKGROUND: Genetic causes of dilated cardiomyopathy (DCM) are incompletely understood. LRRC10 (leucine-rich repeat-containing 10) is a cardiac-specific protein of unknown function. Heterozygous mutations in LRRC10 have been suggested to cause DCM, and deletion of Lrrc10 in mice results in DCM. METHODS AND RESULTS: Whole-exome sequencing was carried out on a patient who presented at 6 weeks of age with DCM and her unaffected parents, filtering for rare, deleterious, recessive, and de novo variants...
February 3, 2018: Journal of the American Heart Association
https://www.readbyqxmd.com/read/29386226/stac3-enhances-expression-of-human-ca-v-1-1-in-xenopus-oocytes-and-reveals-gating-pore-currents-in-hypopp-mutant-channels
#18
Fenfen Wu, Marbella Quinonez, Marino DiFranco, Stephen C Cannon
Mutations of CaV 1.1, the pore-forming subunit of the L-type Ca2+ channel in skeletal muscle, are an established cause of hypokalemic periodic paralysis (HypoPP). However, functional assessment of HypoPP mutant channels has been hampered by difficulties in achieving sufficient plasma membrane expression in cells that are not of muscle origin. In this study, we show that coexpression of Stac3 dramatically increases the expression of human CaV 1.1 (plus α2 -δ1b and β1a subunits) at the plasma membrane of Xenopus laevis oocytes...
January 31, 2018: Journal of General Physiology
https://www.readbyqxmd.com/read/29339150/altered-function-of-neuronal-l-type-calcium-channels-in-ageing-and-neuroinflammation-implications-in-age-related-synaptic-dysfunction-and-cognitive-decline
#19
REVIEW
Sheeja Navakkode, Chao Liu, Tuck Wah Soong
The rapid developments in science have led to an increase in human life expectancy and thus, ageing and age-related disorders/diseases have become one of the greatest concerns in the 21st century. Cognitive abilities tend to decline as we get older. This age-related cognitive decline is mainly attributed to aberrant changes in synaptic plasticity and neuronal connections. Recent studies show that alterations in Ca2+ homeostasis underlie the increased vulnerability of neurons to age-related processes like cognitive decline and synaptic dysfunctions...
March 2018: Ageing Research Reviews
https://www.readbyqxmd.com/read/29338006/a-model-for-cooperative-gating-of-l-type-ca2-channels-and-its-effects-on-cardiac-alternans-dynamics
#20
Daisuke Sato, Rose E Dixon, Luis F Santana, Manuel F Navedo
In ventricular myocytes, membrane depolarization during the action potential (AP) causes synchronous activation of multiple L-type CaV1.2 channels (LTCCs), which trigger the release of calcium (Ca2+) from the sarcoplasmic reticulum (SR). This results in an increase in intracellular Ca2+ (Cai) that initiates contraction. During pulsus alternans, cardiac contraction is unstable, going from weak to strong in successive beats despite a constant heart rate. These cardiac alternans can be caused by the instability of membrane potential (Vm) due to steep AP duration (APD) restitution (Vm-driven alternans), instability of Cai cycling (Ca2+-driven alternans), or both, and may be modulated by functional coupling between clustered CaV1...
January 2018: PLoS Computational Biology
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