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CaV2.2

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https://www.readbyqxmd.com/read/27917413/efficacy-of-s-lacosamide-in-preclinical-models-of-cephalic-pain
#1
Aubin Moutal, Nathan Eyde, Edwin Telemi, Ki Duk Park, Jennifer Y Xie, David W Dodick, Frank Porreca, Rajesh Khanna
Migraine is one of the world's most common neurological disorders. Current acute migraine treatments have sub-optimal efficacy and new therapeutic options are needed. Approaches targeting calcitonin gene related peptide (CGRP) signaling are clinically effective but small molecule antagonists have not been advanced due to toxicity. In this study, we explored the axonal growth/specification collapsin response mediator protein 2 (CRMP2) as a novel "druggable" target for inhibiting CGRP release and for potential relevance for treatment of migraine pain...
June 2016: Pain Reports (Baltimore, Md.)
https://www.readbyqxmd.com/read/27847332/intralipid-protects-the-heart-in-late-pregnancy-against-ischemia-reperfusion-injury-via-caveolin2-stat3-gsk-3%C3%AE-pathway
#2
Jingyuan Li, Gregoire Ruffenach, Georgios Kararigas, Christine M Cunningham, Negar Motayagheni, Neusha Barakai, Soban Umar, Vera Regitz-Zagrosek, Mansoureh Eghbali
BACKGROUND: We recently demonstrated that the heart of late pregnant (LP) rodents is more prone to ischemia/reperfusion (I/R) injury compared to non-pregnant rodents. Lipids, particularly polyunsaturated fatty acids, have received special attention in the field of cardiovascular research. Here, we explored whether Intralipid (ITLD) protects the heart against I/R injury in LP rodents and investigated the mechanisms underlying this protection. METHODS AND RESULTS: In-vivo female LP rat hearts or ex-vivo isolated Langendorff-perfused LP mouse hearts were subjected to ischemia followed by reperfusion with PBS or ITLD (one bolus of 5mg/kg of 20% in in-vivo and 1% in ex-vivo)...
November 12, 2016: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/27843503/review-cav2-3-r-type-voltage-gated-ca-2-channels-functional-implications-in-convulsive-and-non-convulsive-seizure-activity
#3
Carola Wormuth, Andreas Lundt, Christina Henseler, Ralf Müller, Karl Broich, Anna Papazoglou, Marco Weiergräber
BACKGROUND: Researchers have gained substantial insight into mechanisms of synaptic transmission, hyperexcitability, excitotoxicity and neurodegeneration within the last decades. Voltage-gated Ca(2+) channels are of central relevance in these processes. In particular, they are key elements in the etiopathogenesis of numerous seizure types and epilepsies. Earlier studies predominantly targeted on Cav2.1 P/Q-type and Cav3.2 T-type Ca(2+) channels relevant for absence epileptogenesis. Recent findings bring other channels entities more into focus such as the Cav2...
2016: Open Neurology Journal
https://www.readbyqxmd.com/read/27799552/calcium-sensor-regulation-of-the-cav2-1-ca2-channel-contributes-to-long-term-potentiation-and-spatial-learning
#4
Evanthia Nanou, Todd Scheuer, William A Catterall
Many forms of short-term synaptic plasticity rely on regulation of presynaptic voltage-gated Ca(2+) type 2.1 (CaV2.1) channels. However, the contribution of regulation of CaV2.1 channels to other forms of neuroplasticity and to learning and memory are not known. Here we have studied mice with a mutation (IM-AA) that disrupts regulation of CaV2.1 channels by calmodulin and related calcium sensor proteins. Surprisingly, we find that long-term potentiation (LTP) of synaptic transmission at the Schaffer collateral-CA1 synapse in the hippocampus is substantially weakened, even though this form of synaptic plasticity is thought to be primarily generated postsynaptically...
November 15, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27782881/proteolytic-maturation-of-%C3%AE-2%C3%AE-represents-a-checkpoint-for-activation-and-neuronal-trafficking-of-latent-calcium-channels
#5
Ivan Kadurin, Laurent Ferron, Simon W Rothwell, James O Meyer, Leon R Douglas, Claudia S Bauer, Beatrice Lana, Wojciech Margas, Orpheas Alexopoulos, Manuela Nieto-Rostro, Wendy S Pratt, Annette C Dolphin
The auxiliary α2δ subunits of voltage-gated calcium channels are extracellular membrane-associated proteins, which are post-translationally cleaved into disulfide-linked polypeptides α2 and δ. We now show, using α2δ constructs containing artificial cleavage sites, that this processing is an essential step permitting voltage-dependent activation of plasma membrane N-type (CaV2.2) calcium channels. Indeed, uncleaved α2δ inhibits native calcium currents in mammalian neurons. By inducing acute cell-surface proteolytic cleavage of α2δ, voltage-dependent activation of channels is promoted, independent from the trafficking role of α2δ...
October 26, 2016: ELife
https://www.readbyqxmd.com/read/27720444/calcium-calmodulin-dependent-serine-protein-kinase-cask-modulates-the-l-type-calcium-current
#6
Sabine Nafzger, Jean-Sebastien Rougier
AIM: The L-type voltage-gated calcium channel Cav1.2 mediates the calcium influx into cells upon membrane depolarization. The list of cardiopathies associated to Cav1.2 dysfunctions highlights the importance of this channel in cardiac physiology. Calcium/calmodulin-dependent serine protein kinase (CASK), expressed in cardiac cells, has been identified as a regulator of Cav2.2 channels in neurons, but no experiments have been performed to investigate its role in Cav1.2 regulation. METHODS AND RESULTS: Full length or the distal C-terminal truncated of the pore-forming Cav1...
October 5, 2016: Cell Calcium
https://www.readbyqxmd.com/read/27671655/rim-binding-protein-2-regulates-release-probability-by-fine-tuning-calcium-channel-localization-at-murine-hippocampal-synapses
#7
M Katharina Grauel, Marta Maglione, Suneel Reddy-Alla, Claudia G Willmes, Marisa M Brockmann, Thorsten Trimbuch, Tanja Rosenmund, Maria Pangalos, Gülçin Vardar, Alexander Stumpf, Alexander M Walter, Benjamin R Rost, Britta J Eickholt, Volker Haucke, Dietmar Schmitz, Stephan J Sigrist, Christian Rosenmund
The tight spatial coupling of synaptic vesicles and voltage-gated Ca(2+) channels (CaVs) ensures efficient action potential-triggered neurotransmitter release from presynaptic active zones (AZs). Rab-interacting molecule-binding proteins (RIM-BPs) interact with Ca(2+) channels and via RIM with other components of the release machinery. Although human RIM-BPs have been implicated in autism spectrum disorders, little is known about the role of mammalian RIM-BPs in synaptic transmission. We investigated RIM-BP2-deficient murine hippocampal neurons in cultures and slices...
October 11, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27629721/spinal-fbxo3-dependent-fbxl2-ubiquitination-of-active-zone-protein-rim1%C3%AE-mediates-neuropathic-allodynia-through-cav2-2-activation
#8
Cheng-Yuan Lai, Yu-Cheng Ho, Ming-Chun Hsieh, Hsueh-Hsiao Wang, Jen-Kun Cheng, Yat-Pang Chau, Hsien-Yu Peng
UNLABELLED: Spinal plasticity, a key process mediating neuropathic pain development, requires ubiquitination-dependent protein turnover. Presynaptic active zone proteins have a crucial role in regulating vesicle exocytosis, which is essential for synaptic plasticity. Nevertheless, the mechanism for ubiquitination-regulated turnover of presynaptic active zone proteins in the progression of spinal plasticity-associated neuropathic pain remains unclear. Here, after research involving Sprague Dawley rats, we reported that spinal nerve ligation (SNL), in addition to causing allodynia, enhances the Rab3-interactive molecule-1α (RIM1α), a major active zone protein presumed to regulate neural plasticity, specifically in the synaptic plasma membranes (SPMs) of the ipsilateral dorsal horn...
September 14, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27587775/measuring-ca2-dependent-modulation-of-voltage-gated-ca2-channels-in-hek-293t-cells
#9
Jessica R Thomas, Amy Lee
Voltage-gated Ca(2+) (Cav) channels regulate a variety of biological processes, such as muscle contraction, gene expression, and neurotransmitter release. Cav channels are subject to diverse forms of regulation, including those involving the Ca(2+) ions that permeate the pore. High voltage-activated Cav channels undergo Ca(2+)-dependent inactivation (CDI) and facilitation (CDF), which can regulate processes such as cardiac rhythm and synaptic plasticity. CDI and CDF differ slightly between Cav1 (L-type) and Cav2 (P/Q-, N-, and R-type) channels...
September 1, 2016: Cold Spring Harbor Protocols
https://www.readbyqxmd.com/read/27581393/neural-cell-proliferation-and-survival-in-the-hippocampus-of-adult-cav-2-1-calcium-ion-channel-mutant-mice
#10
Fikru Nigussie, Pei-San Huang, Kris Lukauskis, Bhupinder Bawa, Eid Moussa, Louise C Abbott
Tottering mutant mice carry a mutation in the pore-forming subunit (α1A) of CaV2.1 (P/Q-type) voltage-gated calcium ion (Ca(2+)) channels resulting in reduced neuronal Ca(2+) current density. We assessed male tottering mice for spatial learning using the Morris water maze. Tottering mice performed worse than wild type mice, suggesting abnormal hippocampal function. Because Ca(2+) influx via voltage-dependent Ca(2+) channels regulates neuronal survival and function, we assessed hippocampus volume and cell density using hematoxylin and eosin stained serial sections...
November 1, 2016: Brain Research
https://www.readbyqxmd.com/read/27537210/sustained-relief-of-ongoing-experimental-neuropathic-pain-by-a-crmp2-peptide-aptamer-with-low-abuse-potential
#11
Jennifer Y Xie, Lindsey A Chew, Xiaofang Yang, Yuying Wang, Chaoling Qu, Yue Wang, Lauren M Federici, Stephanie D Fitz, Matthew S Ripsch, Michael R Due, Aubin Moutal, May Khanna, Fletcher A White, Todd W Vanderah, Philip L Johnson, Frank Porreca, Rajesh Khanna
Uncoupling the protein-protein interaction between collapsin response mediator protein 2 (CRMP2) and N-type voltage-gated calcium channel (CaV2.2) with an allosteric CRMP2-derived peptide (CBD3) is antinociceptive in rodent models of inflammatory and neuropathic pain. We investigated the efficacy, duration of action, abuse potential, and neurobehavioral toxicity of an improved mutant CRMP2 peptide. A homopolyarginine (R9)-conjugated CBD3-A6K (R9-CBD3-A6K) peptide inhibited the CaV2.2-CRMP2 interaction in a concentration-dependent fashion and diminished surface expression of CaV2...
September 2016: Pain
https://www.readbyqxmd.com/read/27537197/similar-gabaa-receptor-subunit-composition-in-somatic-and-axon-initial-segment-synapses-of-hippocampal-pyramidal-cells
#12
Katalin Kerti-Szigeti, Zoltan Nusser
Hippocampal pyramidal cells (PCs) express many GABAAR subunit types and receive GABAergic inputs from distinct interneurons. Previous experiments revealed input-specific differences in α1 and α2 subunit densities in perisomatic synapses, suggesting distinct IPSC decay kinetics. However, IPSC decays evoked by axo-axonic, parvalbumin- or cholecystokinin-expressing basket cells were found to be similar. Using replica immunogold labeling, here we show that all CA1 PC somatic and AIS synapses contain the α1, α2, β1, β2, β3 and γ2 subunits...
2016: ELife
https://www.readbyqxmd.com/read/27535905/dysregulation-of-neuronal-ca2-channel-linked-to-heightened-sympathetic-phenotype-in-prohypertensive-states
#13
Hege E Larsen, Emma N Bardsley, Konstantinos Lefkimmiatis, David J Paterson
UNLABELLED: Hypertension is associated with impaired nitric oxide (NO)-cyclic nucleotide (CN)-coupled intracellular calcium (Ca(2+)) homeostasis that enhances cardiac sympathetic neurotransmission. Because neuronal membrane Ca(2+) currents are reduced by NO-activated S-nitrosylation, we tested whether CNs affect membrane channel conductance directly in neurons isolated from the stellate ganglia of spontaneously hypertensive rats (SHRs) and their normotensive controls. Using voltage-clamp and cAMP-protein kinase A (PKA) FRET sensors, we hypothesized that impaired CN regulation provides a direct link to abnormal signaling of neuronal calcium channels in the SHR and that targeting cGMP can restore the channel phenotype...
August 17, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27525377/exercise-affects-t-cell-function-via-modifying-intracellular-calcium-homeostasis
#14
Renyi Liu, Wei Fan, Karsten Krüger, Yu Xiao, Christian Pilat, Michael Seimetz, Robert Ringseis, Eveline Baumgart-Vogt, Klaus Eder, Norbert Weissmann, Frank-Christoph Mooren
PURPOSE: The study aimed to investigate the effects of chronic moderate exercise on regulation of intracellular calcium signaling as an important link to proliferation capacity in murine splenic T lymphocytes. METHODS: Male CD1 Swiss mice were randomly assigned either to a control group (CG) or an exercise group (EG). EG mice performed voluntary exercise for 3 months. Lymphocytes were isolated from murine spleens and intracellular calcium was determined using Fura-2(AM) and fluorescence spectrometry...
August 12, 2016: Medicine and Science in Sports and Exercise
https://www.readbyqxmd.com/read/27489103/the-cav%C3%AE-subunit-protects-the-i-ii-loop-of-the-voltage-gated-calcium-channel-cav2-2-from-proteasomal-degradation-but-not-oligoubiquitination
#15
Karen M Page, Simon W Rothwell, Annette C Dolphin
CaVβ subunits interact with the voltage-gated calcium channel CaV2.2 on a site in the intracellular loop between domains I and II (the I-II loop). This interaction influences the biophysical properties of the channel and leads to an increase in its trafficking to the plasma membrane. We have shown previously that a mutant CaV2.2 channel that is unable to bind CaVβ subunits (CaV2.2 W391A) was rapidly degraded (Waithe, D., Ferron, L., Page, K. M., Chaggar, K., and Dolphin, A. C. (2011) J. Biol. Chem. 286, 9598-9611)...
September 23, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27480382/opposite-associations-between-the-rs3845446-single-nucleotide-polymorphism-of-the-cacna1e-gene-and-postoperative-pain-related-phenotypes-in-gastrointestinal-surgery-versus-previously-reported-orthognathic-surgery
#16
Kojiro Amano, Daisuke Nishizawa, Tsutomu Mieda, Miki Tsujita, Akira Kitamura, Junko Hasegawa, Eiichi Inada, Masakazu Hayashida, Kazutaka Ikeda
UNLABELLED: Cav2.3 (R-type) voltage-activated Ca(2+) channels (VACCs), encoded by the calcium channel, voltage-dependent, R-type, α1E subunit (CACNA1E) gene, are responsible for transmission of somatic inflammatory pain, and activation of antinociception elicited by visceral inflammatory pain stimuli. Carriers of the minor G allele of the rs3845446 single-nucleotide polymorphism (SNP) of the CACNA1E gene reportedly exhibit a decrease in opioid requirements to control typical somatic inflammatory pain after orthognathic surgery (ie, a painful cosmetic surgery), suggesting the downregulation of Cav2...
October 2016: Journal of Pain: Official Journal of the American Pain Society
https://www.readbyqxmd.com/read/27468821/redistribution-of-cav2-1-channels-and-calcium-ions-in-nerve-terminals-following-end-to-side-neurorrhaphy-ionic-imaging-analysis-by-tof-sims
#17
Chiung-Hui Liu, Hung-Ming Chang, To-Jung Tseng, Chyn-Tair Lan, Li-You Chen, Su-Chung Youn, Jian-Jr Lee, Fu-Der Mai, Jui-Feng Chou, Wen-Chieh Liao
The P/Q-type voltage-dependent calcium channel (Cav2.1) in the presynaptic membranes of motor nerve terminals plays an important role in regulating Ca(2+) transport, resulting in transmitter release within the nervous system. The recovery of Ca(2+)-dependent signal transduction on motor end plates (MEPs) and innervated muscle may directly reflect nerve regeneration following peripheral nerve injury. Although the functional significance of calcium channels and the levels of Ca(2+) signalling in nerve regeneration are well documented, little is known about calcium channel expression and its relation with the dynamic Ca(2+) ion distribution at regenerating MEPs...
November 2016: Histochemistry and Cell Biology
https://www.readbyqxmd.com/read/27440246/the-ionic-mechanism-of-membrane-potential-oscillations-and-membrane-resonance-in-striatal-lts-interneurons
#18
S C Song, J A Beatty, C J Wilson
Striatal low-threshold spiking (LTS) interneurons spontaneously transition to a depolarized, oscillating state similar to that seen after sodium channels are blocked. In the depolarized state, whether spontaneous or induced by sodium channel blockade, the neurons express a 3- to 7-Hz oscillation and membrane impedance resonance in the same frequency range. The membrane potential oscillation and membrane resonance are expressed in the same voltage range (greater than -40 mV). We identified and recorded from LTS interneurons in striatal slices from a mouse that expressed green fluorescent protein under the control of the neuropeptide Y promoter...
October 1, 2016: Journal of Neurophysiology
https://www.readbyqxmd.com/read/27430911/baicalein-a-constituent-of-scutellaria-baicalensis-reduces-glutamate-release-and-protects-neuronal-cell-against-kainic-acid-induced-excitotoxicity-in-rats
#19
Yi Chang, Cheng Wei Lu, Tzu Yu Lin, Shu Kuei Huang, Su Jane Wang
Interest in the health benefits of flavonoids, particularly their effects on neurodegenerative disease, is increasing. This study evaluated the role of baicalein, a flavonoid compound isolated from the traditional Chinese medicine Scutellaria baicalensis, in glutamate release and glutamate neurotoxicity in the rat hippocampus. In the rat hippocampal nerve terminals (synaptosomes), baicalein inhibits depolarization-induced glutamate release, and this phenomenon is prevented by chelating the extracellular Ca[Formula: see text] ions and blocking presynaptic Cav2...
2016: American Journal of Chinese Medicine
https://www.readbyqxmd.com/read/27426949/presynaptic-excitation-via-gabab-receptors-in-habenula-cholinergic-neurons-regulates-fear-memory-expression
#20
Juen Zhang, Lubin Tan, Yuqi Ren, Jingwen Liang, Rui Lin, Qiru Feng, Jingfeng Zhou, Fei Hu, Jing Ren, Chao Wei, Tao Yu, Yinghua Zhuang, Bernhard Bettler, Fengchao Wang, Minmin Luo
Fear behaviors are regulated by adaptive mechanisms that dampen their expression in the absence of danger. By studying circuits and the molecular mechanisms underlying this adaptive response, we show that cholinergic neurons of the medial habenula reduce fear memory expression through GABAB presynaptic excitation. Ablating these neurons or inactivating their GABAB receptors impairs fear extinction in mice, whereas activating the neurons or their axonal GABAB receptors reduces conditioned fear. Although considered exclusively inhibitory, here, GABAB mediates excitation by amplifying presynaptic Ca(2+) entry through Cav2...
July 28, 2016: Cell
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