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https://www.readbyqxmd.com/read/29246857/new-cav2-calcium-channel-gating-modifiers-with-agonist-activity-and-therapeutic-potential-to-treat-neuromuscular-disease
#1
Man Wu, Hayley V White, Blake Boehm, Christopher J Meriney, Kaylan Kerrigan, Michael Frasso, Mary Liang, Erika M Gotway, Madeleine Wilcox, Jon W Johnson, Peter Wipf, Stephen D Meriney
Voltage-gated calcium channels (VGCCs) are critical regulators of many cellular functions, including the activity-dependent release of chemical neurotransmitter from nerve terminals. At nerve terminals, the Cav2 family of VGCCs are closely positioned with neurotransmitter-containing synaptic vesicles. The relationship between calcium ions and transmitter release is such that even subtle changes in calcium flux through VGCCs have a strong influence on the magnitude of transmitter released. Therefore, modulators of the calcium influx at nerve terminals have the potential to strongly affect transmitter release at synapses...
December 12, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/29237755/differential-contribution-of-ca2-sources-to-day-and-night-bk-current-activation-in-the-circadian-clock
#2
Joshua P Whitt, Beth A McNally, Andrea L Meredith
Large conductance K+ (BK) channels are expressed widely in neurons, where their activation is regulated by membrane depolarization and intracellular Ca2+ (Ca2+i). To enable this regulation, BK channels functionally couple to both voltage-gated Ca2+ channels (VGCCs) and channels mediating Ca2+ release from intracellular stores. However, the relationship between BK channels and their specific Ca2+ source for particular patterns of excitability is not well understood. In neurons within the suprachiasmatic nucleus (SCN)-the brain's circadian clock-BK current, VGCC current, and Ca2+i are diurnally regulated, but paradoxically, BK current is greatest at night when VGCC current and Ca2+i are reduced...
December 13, 2017: Journal of General Physiology
https://www.readbyqxmd.com/read/29189554/paraneoplastic-lambert-eaton-myasthenic-syndrome-with-limbic-encephalitis-clinical-correlation-with-the-coexistence-of-anti-vgcc-and-anti-gabab-receptor-antibodies
#3
Jonathan J Cho, James P Wymer
OBJECTIVE: To characterize Lambert-Eaton myasthenic syndrome and limbic encephalitis with coexistent voltage-gated calcium channel (VGCC) antibody and γ-aminobutyric acid (GABA) B receptor antibody. METHODS: Case study. RESULTS: A 57-year-old man presented with 6 months of weakness, unsteadiness, and vision difficulties. Examination revealed proximal weakness and diminished reflexes. Electrodiagnostic study revealed low-amplitude motor potentials and facilitation on high-frequency stimulation...
December 2017: Journal of Clinical Neuromuscular Disease
https://www.readbyqxmd.com/read/29166605/l-type-voltage-gated-ca2-channels-regulate-synaptic-activity-triggered-recycling-endosome-fusion-in-neuronal-dendrites
#4
Brian G Hiester, Ashley M Bourke, Brooke L Sinnen, Sarah G Cook, Emily S Gibson, Katharine R Smith, Matthew J Kennedy
The repertoire and abundance of proteins displayed on the surface of neuronal dendrites are tuned by regulated fusion of recycling endosomes (REs) with the dendritic plasma membrane. While this process is critical for neuronal function and plasticity, how synaptic activity drives RE fusion remains unexplored. We demonstrate a multistep fusion mechanism that requires Ca2+ from distinct sources. NMDA receptor Ca2+ initiates RE fusion with the plasma membrane, while L-type voltage-gated Ca2+ channels (L-VGCCs) regulate whether fused REs collapse into the membrane or reform without transferring their cargo to the cell surface...
November 21, 2017: Cell Reports
https://www.readbyqxmd.com/read/29158500/use-dependent-potentiation-of-voltage-gated-calcium-channels-rescues-neurotransmission-in-nerve-terminals-intoxicated-by-botulinum-neurotoxin-serotype-a
#5
Phillip H Beske, Katie M Hoffman, James B Machamer, Margaret R Eisen, Patrick M McNutt
Botulinum neurotoxins (BoNTs) are highly potent toxins that cleave neuronal SNARE proteins required for neurotransmission, causing flaccid paralysis and death by asphyxiation. Currently, there are no clinical treatments to delay or reverse BoNT-induced blockade of neuromuscular transmission. While aminopyridines have demonstrated varying efficacy in transiently reducing paralysis following BoNT poisoning, the precise mechanisms by which aminopyridines symptomatically treat botulism are not understood. Here we found that activity-dependent potentiation of presynaptic voltage-gated calcium channels (VGCCs) underlies 3,4-diaminopyridine (3,4-DAP)-mediated rescue of neurotransmission in central nervous system synapses and mouse diaphragm neuromuscular junctions fully intoxicated by BoNT serotype A...
November 20, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29137729/the-shear-wave-elastic-modulus-and-the-increased-nuclear-factor-kappa-b-nf-kb-p65-and-cyclooxygenase-2-cox-2-expression-in-the-area-of-myofascial-trigger-points-activated-in-a-rat-model-by-blunt-trauma-to-the-vastus-medialis
#6
Hengyong Lv, Zhen Li, Tiantian Hu, Yuexiang Wang, Jinpeng Wu, Yingxin Li
We aimed to elucidate the increased inflammatory cytokines expression such as nuclear factor kappa B (NF-kB/p65), cyclooxygenase-2 (COX-2), and voltage-gated calcium channels (VGCC) in the area of activated myofascial trigger points (MTrPs) in a rat model by blunt trauma to the vastus medialis and to evaluate the feasibility of a quantitative analysis of muscle elastic modulus using shear wave elastography (SWE). Twelve 7-week-old male SD rats were divided into normal (NM, n = 6) and model groups (MO, n = 6)...
November 6, 2017: Journal of Biomechanics
https://www.readbyqxmd.com/read/29125390/responsiveness-of-voltage-gated-calcium-channels-in-sh-sy5y-human-neuroblastoma-cells-on-micropillar-substrates
#7
Wenxu Wang, Donghuo Zhong, Yu Lin, Rong Fan, Zhengjun Hou, Xiumei Cao, Yubin Ren
In this study, poly-L-lactic acid (PLLA) micropillar substrates were fabricated to evaluate the influence of topographic substrates on cell morphological and functional characteristics, such as spreading area, voltage-gated calcium channels (VGCCs) and membrane potential. The proliferation, spreading area, perimeter and circularity of SH-SY5Y cells interfaced with different substrates were first investigated. In addition, the cytoskeleton and focal adhesion of a cell as important manifestations of cell morphology were analyzed by immunofluorescence...
November 10, 2017: Journal of Biomaterials Science. Polymer Edition
https://www.readbyqxmd.com/read/29061745/mechanism-of-action-of-miltefosine-on-leishmania-donovani-involves-the-impairment-of-acidocalcisomes-function-and-the-activation-of-the-sphingosine-dependent-plasma-membrane-ca-2-channel
#8
Andrea K Pinto-Martinez, Jessica Rodriguez-Durán, Xenon Serrano-Martin, Vanessa Hernandez-Rodriguez, Gustavo Benaim
Leishmania donovani is the causing agent of visceral leishmaniasis, a common infection that affects millions of people from the most underdeveloped countries. Miltefosine is the only oral drug to treat infections caused by L. donovani. Nevertheless, its mechanism of action is not well understood. While miltefosine inhibits the synthesis of phosphatidylcholine, and also affects the parasite mitochondrion inhibiting the cytochrome C oxidase, it is to be expected that this potent drug also produces its effect through other targets...
October 23, 2017: Antimicrobial Agents and Chemotherapy
https://www.readbyqxmd.com/read/29054436/in-vitro-and-ex-vivo-screening-of-candidate-therapeutics-to-restore-neurotransmission-in-nerve-terminals-intoxicated-by-botulinum-neurotoxin-serotype-a1
#9
Phillip H Beske, Aaron B Bradford, Katie M Hoffman, Sydney Mason, Patrick M McNutt
Botulinum neurotoxins (BoNTs) are exceedingly potent neurological poisons that block cholinergic release in the peripheral nervous system and cause death by asphyxiation. While post-exposure prophylaxis can effectively eliminate toxin in the bloodstream, there are no clinically effective treatments to prevent or reverse disease once BoNT has entered the neuron. To address the need for post-symptomatic countermeasures, we designed and developed an in vitro assay based on whole-cell, patch-clamp electrophysiological monitoring of miniature excitatory post-synaptic currents in synaptically active murine embryonic stem cell-derived neurons...
October 17, 2017: Toxicon: Official Journal of the International Society on Toxinology
https://www.readbyqxmd.com/read/29042437/posttranslational-processing-and-membrane-translocation-of-the-yeast-regulatory-mid1-subunit-of-the-cch1-vgcc-nalcn-cation-channel-family
#10
Kazuko Iida, Jinfeng Teng, Toshihiko Cho, Sato Yoshikawa-Kimura, Hidetoshi Iida
Saccharomyces cerevisiae Mid1 is composed of 548 amino acids and a regulatory subunit of Cch1, a member of the eukaryotic pore-forming, four-domain cation channel family. The amino acid sequence and voltage insensitivity of Cch1 are more similar to those of Na+ leak channel non-selective (NALCN) than to the α1 subunit of voltage-gated Ca2+ channels (VGCCs). Despite a lack in overall primary sequence similarity, Mid1 resembles in some aspects VGCC α2/δ regulatory subunits and NALCN-associated proteins. Unlike animal α2/δ subunits, Mid1 and NALCN-associated proteins are essential for the function of the pore-forming subunit...
October 17, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29020622/homeostatic-presynaptic-plasticity-is-specifically-regulated-by-p-q-type-ca-2-channels-at-mammalian-hippocampal-synapses
#11
Alexander F Jeans, Fran C van Heusden, Bashayer Al-Mubarak, Zahid Padamsey, Nigel J Emptage
Voltage-dependent Ca(2+) channels (VGCC) represent the principal source of Ca(2+) ions driving evoked neurotransmitter release at presynaptic boutons. In mammals, presynaptic Ca(2+) influx is mediated mainly via P/Q-type and N-type VGCC, which differ in their properties. Changes in their relative contributions tune neurotransmission both during development and in Hebbian plasticity. However, whether this represents a functional motif also present in other forms of activity-dependent regulation is unknown. Here, we study the role of VGCC in homeostatic plasticity (HSP) in mammalian hippocampal neurons using optical techniques...
October 10, 2017: Cell Reports
https://www.readbyqxmd.com/read/28992975/a-prospective-placebo-controlled-study-on-the-humoral-immune-response-to-and-safety-of-tetanus-revaccination-in-myasthenia-gravis
#12
Ellen Strijbos, Maartje G Huijbers, Inge E van Es, Iris Alleman, Monique M van Ostaijen-Ten Dam, Jaap Bakker, Erik W van Zwet, Cornelia M Jol-van der Zijde, Maarten D van Tol, Jan J Verschuuren
OBJECTIVE: To investigate the humoral immune response to and safety of a tetanus revaccination in patients with myasthenia gravis or Lambert-Eaton myasthenic syndrome. METHODS: A tetanus revaccination was administered to 66 patients. Before and 4weeks after revaccination a blood sample and clinical outcome scores were obtained. Anti-tetanus IgG total, IgG1 and IgG4 titres were measured with an ELISA and disease-specific antibody titres (AChR, MuSK or VGCC) with a radio-immunoprecipitation assay...
October 6, 2017: Vaccine
https://www.readbyqxmd.com/read/28990373/sigma-1-receptor-agonist-increases-axon-outgrowth-of-hippocampal-neurons-via-voltage-gated-calcium-ions-channels
#13
Dong Li, Shu-Zhuo Zhang, Yu-Hong Yao, Yun Xiang, Xiao-Yun Ma, Xiao-Li Wei, Hai-Tao Yan, Xiao-Yan Liu
INTRODUCTION: Sigma-1 receptors (Sig-1Rs) are unique endoplasmic reticulum proteins that have been implicated in both neurodegenerative and ischemic diseases, such as Alzheimer's disease and stroke. Accumulating evidence has suggested that Sig-1R plays a role in neuroprotection and axon outgrowth. The underlying mechanisms of Sig-1R-mediated neuroprotection have been well elucidated. However, the mechanisms underlying the effects of Sig-1R on axon outgrowth are not fully understood. METHODS: To clarify this issue, we utilized immunofluorescence to compare the axon lengths of cultured naïve hippocampal neurons before and after the application of the Sig-1R agonist, SA4503...
October 8, 2017: CNS Neuroscience & Therapeutics
https://www.readbyqxmd.com/read/28978758/targeting-of-photoreceptor-genes-in-chlamydomonas-reinhardtii-via-zinc-finger-nucleases-and-crispr-cas9
#14
Andre Greiner, Simon Kelterborn, Heide Evers, Georg Kreimer, Irina Sizova, Peter Hegemann
The fast-growing biflagellated single celled chlorophyte Chlamydomonas reinhardtii is the most widely used alga in basic research. The physiological functions of the 18 sensory photoreceptors are of particular interest with respect to C. reinhardtii development and behavior. Despite the demonstration of gene editing in C. reinhardtii in 1995, the isolation of mutants lacking easily ascertained newly acquired phenotypes remains problematic due to low DNA recombination efficiency. We optimized gene-editing protocols for several Chlamydomonas strains (including wild-type CC-125) using zinc-finger nucleases (ZFNs), genetically encoded CRISPR/associated protein 9 (Cas9) from Staphylococcus aureus and Streptococcus pyogenes, and recombinant Cas9 and developed protocols for rapidly isolating non-selectable gene mutants...
October 4, 2017: Plant Cell
https://www.readbyqxmd.com/read/28945273/vpac1-and-vpac2-receptor-opposed-modulation-of-gaba-release-from-hippocampal-nerve-terminals-involves-multiple-signalling-pathways
#15
Diana Cunha-Reis, Joaquim Alexandre Ribeiro, Rodrigo F M de Almeida, Ana M Sebastião
BACKGROUND AND PURPOSE: Vasoactive intestinal peptide (VIP) is an important modulator of hippocampal synaptic transmission that influences both GABAergic synaptic transmission and glutamatergic cell excitability through activation of VPAC1 and VPAC2 receptors. Presynaptic enhancement of GABA release contributes to VIP modulation of hippocampal synaptic transmission. EXPERIMENTAL APPROACH: We now investigated which VIP receptors and coupled transduction pathways are involved in VIP enhancement of K(+) -evoked [(3) H]-GABA) release from rat hippocampal isolated nerve terminals...
September 25, 2017: British Journal of Pharmacology
https://www.readbyqxmd.com/read/28930822/five-years-experience-on-3-4-diaminopyridine-phosphate-in-lambert-eaton-syndrome-case-reports
#16
Simona Portaro, Teresa Brizzi, Stefano Sinicropi, Alberto Cacciola, Maria Cristina De Cola, Alessia Bramanti, Demetrio Milardi, Antonino Lupica, Placido Bramanti, Antonio Toscano, Carmelo Rodolico
RATIONALE: To report our experience on 7 patients (4 males and 3 females), affected by nonparaneoplastic Lambert-Eaton myasthenic syndrome, treated with 3,4-diaminopyridine phosphate (3,4-DAPP) either alone or in combination with other immunosuppressants or steroids. PATIENT CONCERNS: Patients have been evaluated at specific timepoints (ie, baseline and last 5 year follow-up), with neurological examination, autoantibodies against presynaptic voltage-gated Cav2.1 (P/Q type) calcium ion channel (VGCC) dosage, neurophysiological evaluation focusing on the increased amplitude of the compound muscle action potential (cMAP) after maximum voluntary effort, quantitative myasthenia gravis (QMG) and activities of daily living scales, and autonomic nervous system involvement evaluation...
September 2017: Medicine (Baltimore)
https://www.readbyqxmd.com/read/28921719/inflammation-alters-ampa-stimulated-calcium-responses-in-dorsal-striatal-d2-but-not-d1-spiny-projection-neurons
#17
Carissa D Winland, Nora Welsh, Alberto Sepulveda-Rodriguez, Stefano Vicini, Kathleen A Maguire-Zeiss
Neuroinflammation precedes neuronal loss in striatal neurodegenerative diseases and can be exacerbated by the release of proinflammatory molecules by microglia. These molecules can affect trafficking of AMPARs. The preferential trafficking of calcium-permeable versus impermeable AMPARs can result in disruptions of [Ca(2+) ]i and alter cellular functions. In striatal neurodegenerative diseases, changes in [Ca(2+) ]i and L-type voltage-gated calcium channels (VGCCs) have been reported. Therefore, this study sought to determine whether a proinflammatory environment alters AMPA-stimulated [Ca(2+) ]i through calcium-permeable AMPARs and/or L-type VGCCs in dopamine-2- and dopamine-1-expressing striatal spiny projection neurons (D2 and D1 SPNs) in the dorsal striatum...
November 2017: European Journal of Neuroscience
https://www.readbyqxmd.com/read/28899915/conditional-deletion-of-the-l-type-calcium-channel-cav1-2-in-ng2-positive-cells-impairs-remyelination-in-mice
#18
Diara A Santiago González, Veronica T Cheli, Norma N Zamora, Tenzing N Lama, Vilma Spreuer, Geoffrey G Murphy, Pablo M Paez
Exploring the molecular mechanisms that drive the maturation of oligodendrocyte progenitor cells (OPCs) during the remyelination process is essential to developing new therapeutic tools to intervene in demyelinating diseases such as multiple sclerosis. To determine whether L-type voltage-gated calcium channels (L-VGCCs) are required for OPC development during remyelination, we generated an inducible conditional knock-out mouse in which the L-VGCC isoform Cav1.2 was deleted in NG2-positive OPCs (Cav1.2(KO))...
October 18, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28867800/ciguatoxins-evoke-potent-cgrp-release-by-activation-of-voltage-gated-sodium-channel-subtypes-nav1-9-nav1-7-and-nav1-1
#19
Filip Touska, Simon Sattler, Philipp Malsch, Richard J Lewis, Peter W Reeh, Katharina Zimmermann
Ciguatoxins (CTXs) are marine toxins that cause ciguatera fish poisoning, a debilitating disease dominated by sensory and neurological disturbances that include cold allodynia and various painful symptoms as well as long-lasting pruritus. Although CTXs are known as the most potent mammalian sodium channel activator toxins, the etiology of many of its neurosensory symptoms remains unresolved. We recently described that local application of 1 nM Pacific Ciguatoxin-1 (P-CTX-1) into the skin of human subjects induces a long-lasting, painful axon reflex flare and that CTXs are particularly effective in releasing calcitonin-gene related peptide (CGRP) from nerve terminals...
August 30, 2017: Marine Drugs
https://www.readbyqxmd.com/read/28862523/l-and-t-type-calcium-channel-blockers-protect-against-the-inhibitory-effects-of-mipafox-on-neurite-outgrowth-and-plasticity-related-proteins-in-sh-sy5y-cells
#20
Laís Silva Fernandes, Neife Aparecida G Dos Santos, Guilherme Luz Emerick, Antonio Cardozo Dos Santos
Some organophosphorus compounds (OP), including the pesticide mipafox, produce late onset distal axonal degeneration, known as organophosphorus-induced delayed neuropathy (OPIDN). The underlying mechanism involves irreversible inhibition of neuropathy target esterase (NTE) activity, elevated intracellular calcium levels, increased activity of calcium-activated proteases and impaired neuritogenesis. Voltage-gated calcium channels (VGCC) appear to play a role in several neurologic disorders, including OPIDN. Therefore, this study aimed to examine and compare the neuroprotective effects of T-type (amiloride) and L-type (nimodipine) VGCC blockers induced by the inhibitory actions of mipafox on neurite outgrowth and axonal proteins of retinoic-acid-stimulated SH-SY5Y human neuroblastoma cells, a neuronal model widely employed to determine the neurotoxicity attributed to OP...
September 1, 2017: Journal of Toxicology and Environmental Health. Part A
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