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82 results for “calcium channel”
Inhibition of striatal dopamine release by the L-type calcium channel inhibitor isradipine co-varies with risk factors for Parkinson's
<h3><strong>ABSTRACT</strong></h3> <p>Ca<sup>2+</sup> entry into nigrostriatal dopamine (DA) neurons and axons via L-type voltage-gated Ca<sup>2+</sup> channels (LTCCs) contributes respectively to pacemaker activity and DA release, and has long been thought to contribute to vulnerability to degeneration in Parkinson’s disease. LTCC function is greater in DA axons and neurons from substantia nigra pars compacta than from ventral tegmental area, but this is not explained by channel expression level. We tested the hypothesis that LTCC-control of DA release is governed rather by local mechanisms, focussing on candidate biological factors known to operate differently between types of DA neurons and/or be associated with their differing vulnerability to parkinsonism, including biological sex, α-synuclein, DA transporters (DATs), and calbindin-D28k (Calb1). We detected evoked DA release <em>ex vivo </em>in mouse striatal slices using fast-scan cyclic voltammetry, and assessed LTCC support of DA release by detecting the inhibition of DA release by the LTCC inhibitors isradipine or CP8. Using genetic knockouts or pharmacological manipulations we identified that striatal LTCC support of DA release depended on multiple intersecting factors, in a regionally and sexually divergent manner. LTCC function was promoted by factors associated with Parkinsonian risk, including male sex, α-synuclein, DAT, and a dorsolateral co-ordinate, but limited by factors associated with protection i.e. female sex, glucocerebrosidase activity, Calb1, and ventromedial co-ordinate. Together, these data show that LTCC function in DA axons, and isradipine effect, are locally governed and suggest they vary in a manner that in turn might impact on, or reflect, the cellular stress that leads to parkinsonian degeneration.</p> <p> </p> <h3><strong>FILE DESCRIPTIONS</strong></h3> <p>This repository contains the following files:</p> <ul> <li>Key Resources Table (.xlsx) - Table containing details on key lab materials (antibodies, mouse lines, and software), and the persistent identifiers for protocols and code used and generated in this study. </li> <li>Source Data (.xlsx) - Excel spreadsheet containing all tabular datasets plotted in Main Figures 1 to 5 (.xlsx).</li> <li>R_Scritps (.R) - Custom written R scripts to perform a classification tree analysis.</li> </ul>
Calcium channel model
<p>This dataset contains two data tables, include "channel_model.mat", "U_potential_3D_e(60).mat". The first data table is used to construct 2D and 3D calcium channel models. The model is constructed based on the model in the Ref. (Corry et al., 2001). The second data table gives the potential distribution in 3D calcium ion channels for Brownian dynamics calculation of ion transport in calcium ion channels.</p>
Data from: Nonlinearities between inhibition and T-type calcium channel activity bidirectionally regulate thalamic oscillations
<p>Absence seizures result from 3-5 Hz generalized thalamocortical oscillations that depend on highly regulated inhibitory neurotransmission in the thalamus. Efficient reuptake of the inhibitory neurotransmitter GABA is essential, and reuptake failure worsens seizures. Here, we show that blocking GABA transporters (GATs) in acute brain slices containing key parts of the thalamocortical seizure network modulates epileptiform activity. As expected, we found that blocking either GAT1 or GAT3 prolonged oscillations. However, blocking both GATs unexpectedly suppressed oscillations. Integrating experimental observations into single-neuron and network-level computational models shows how a non-linear dependence of T-type calcium channel opening on GABA<sub>B</sub> receptor activity regulates network oscillations. Receptor activity that is either too brief or too protracted fails to sufficiently open T-type channels necessary for sustaining oscillations. Only within a narrow range does prolonging GABA<sub>B</sub> receptor activity promote channel opening and intensify oscillations. These results have implications for therapeutics that modulate GABA transporters.</p>
Mapping the interaction surface between CaVβ and actin and its role in calcium channel clearance
<p><strong>HADDOCK protein-protein docking data for the Ca<sub>V</sub>β/F-actin complex models reported in "Mapping the interaction surface between Ca<sub>V</sub>β and actin and its role in calcium channel clearance".</strong></p> <p> </p> <p>The dataset is divided in four different folders:</p> <ol> <li><strong>Cavbeta2:</strong> data for the docking between dimeric actin (PDB 5OOE) and Ca<sub>V</sub>β<sub>2</sub> (PDB 5V2P) using XL-MS-derived distance restraints </li> <li><strong>Cavbeta4:</strong> data for the docking between dimeric actin (PDB 5OOE) and Ca<sub>V</sub>β<sub>4</sub> (PDB 1VYV) using XL-MS-derived distance restraints </li> <li><strong>Monomer:</strong> data for the control docking between <em>monomeric</em> actin (PDB 5OOE) and Ca<sub>V</sub>β<sub>2</sub> (PDB 5V2P) using XL-MS-derived distance restraints </li> <li><strong>Ab_initio:</strong> data for the control dockings between dimeric actin (PDB 5OOE) and Ca<sub>V</sub>β<sub>2</sub> (PDB 5V2P) <em>without</em> XL-MS-derived distance restraints and using the <em>ab initio</em> options available in HADDOCK 2.4</li> </ol> <p> </p> <p>Each of the <strong>Cavbeta</strong> folders (1-2) and the <strong>Monomer</strong> folder (3) contain:</p> <p>- Inputs: </p> <ul> <li>HADDOCK run parameter file (job_params.json)</li> <li>XL/MS-derived unambiguous distance restraints (unambig.tbl)</li> <li>Bioinformatics-derived (CPORT and NACCESS) ambiguous distance restraints (ambig.tbl)</li> </ul> <p>- Outputs:</p> <ul> <li>Top 4 models of the selected HADDOCK cluster (cluster1_1.pdb, ..., cluster1_4.pdb)</li> <li>Source data for the docking analyses presented in the Supplementary Information (Supplementary Figures 4, 6, 9, 13 and 14 and Supplementary Table 4)</li> </ul> <p> </p> <p>The <strong>Ab_initio</strong> folder (4) contains:</p> <p>- Input: </p> <ul> <li>HADDOCK run parameter files for each of the six control simulations presented in Supplementary Table 6 (job_params.json)</li> </ul> <p>- Outputs:</p> <ul> <li>Source data for the docking analyses presented in Supplementary Table 6</li> <li>Model from control simulation 1 shown in Supplementary Figure 5</li> </ul> <p> </p>
Simultaneous two-photon voltage or calcium imaging and multi-channel LFP recordings in barrel cortex of awake and anesthetized mice
<p>Neuronal population activity, both spontaneous and sensory-evoked, generates propagating waves in cortex. However, high spatiotemporal-resolution mapping of these waves is difficult as calcium imaging, the work horse of current imaging, does not reveal subthreshold activity.</p> <p>Here, we present a platform combining voltage or calcium two-photon imaging with multi-channel local field potential (LFP) recordings in different layers of the barrel cortex from anesthetized and awake head-restrained mice. A chronic cranial window with access port allows injecting a viral vector expressing GCaMP6f or the voltage-sensitive dye (VSD) ANNINE-6plus, as well as entering the brain with a multi-channel neural probe. We present both average spontaneous activity and average evoked signals in response to multi-whisker air-puff stimulations.</p> <p>Time domain analysis shows the dependence of the evoked responses on the cortical layer and on the state of the animal, here separated into anesthetized, awake but resting, and running. The simultaneous data acquisition allows to compare the average membrane depolarization measured with ANNINE-6plus with the amplitude and shape of the LFP recordings. The calcium imaging data connects these data sets to the large existing database of this important second messenger. Interestingly, in the calcium imaging data, we found a few cells which showed a decrease in calcium concentration in response to vibrissa stimulation in awake mice.</p> <p>This system offers a multimodal technique to study the spatiotemporal dynamics of neuronal signals through a 3D architecture in vivo. It will provide novel insights on sensory coding, closing the gap between electrical and optical recordings.</p>
Cytosolic peptides encoding CaV1 C-termini downregulate the calcium channel activity-neuritogenesis coupling
<p><span>L-type Ca<sup>2+</sup> (Ca<sub>V</sub>1) channels transduce channel activities into nuclear signals critical to neuritogenesis. Also, standalone peptides encoded by </span><span><span>Ca<sub>V</sub>1</span> DCT (distal carboxyl-terminus) act as nuclear transcription factors reportedly promoting neuritogenesis. Here, by focusing on exemplary </span><span><span>Ca<sub>V</sub>1</span>.3 and cortical neurons under basal conditions, we discover that cytosolic DCT peptides downregulate neurite outgrowth by the interactions with </span><span><span>Ca<sub>V</sub>1</span>'s apo-calmodulin binding motif. Distinct from nuclear DCT, various cytosolic peptides exert a gradient of inhibitory effects on </span><span>Ca<sup>2+</sup></span><span> influx via CaV1 channels and neurite extension and arborization, and also the intermediate events including CREB activation and c-Fos expression. The inhibition efficacies of DCT are quantitatively correlated with its binding affinities. Meanwhile, c</span><span>ytosolic inhibition tends to facilitate neuritogenesis indirectly by favoring </span><span>Ca<sup>2+</sup>-sensitive nuclear retention of DCT. In summary, DCT peptides as a class of </span><span><span>Ca<sub>V</sub>1</span> inhibitors specifically regulate the channel activity-neuritogenesis coupling in a variant-, affinity-, and localization-dependent manner.</span></p>
The intracellular C-terminus confers compartment-specific targeting of voltage-gated calcium channels
<p>This table contains all tabulated data for:</p> <p>Chin and Kaeser, 2024. "The intracellular C-terminus confers compartment-specific targeting of voltage-gated calcium channels."</p> <p>Detailed methods are provided in the paper. </p>
Aliskiren and the Calcium Channel Blocker Amlodipine Combination as an Initial Treatment Strategy for Hypertension
ClinicalTrials.gov study NCT00797862. IPD Sharing: Not stated. Countries: 10. Publications: 2.
Efficacy Study of PDE-5 Inhibitor and Calcium Channel Inhibitor for the Treatment of Secondary Raynaud Phenomenon
ClinicalTrials.gov study NCT01280266. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Assessing the Impact of Calcium Channel Blockers on COGnitive Function in the Very Elderly (AI-COG)
ClinicalTrials.gov study NCT01868165. IPD Sharing: NO. Countries: 1. Publications: 1.
BLOCKade of Calcium Channels and Beta Adrenergic Receptors for the Treatment of Hypertension in HFpEF
ClinicalTrials.gov study NCT04434664. IPD Sharing: Not stated. Countries: 1. Publications: 8.
Data from: Nonlinearities between inhibition and T-type calcium channel activity bidirectionally regulate thalamic oscillations
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Cytosolic peptides encoding CaV1 C-termini downregulate the calcium channel activity-neuritogenesis coupling
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Simultaneous two-photon voltage or calcium imaging and multi-channel LFP recordings in barrel cortex of awake and anesthetized mice
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Data from: Diethylcarbamazine elicits calcium signals in HEK293 cells by activation of heterologously expressed <em>Brugia malayi</em> TRP-2b channels
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Learning Implementation of Guideline-based Decision Support System for Hypertension Treatment: Testing Alternative Antihypertensive Regimens Using ACE-Inhibitors, Calcium Channel Blockers and Diuretic
ClinicalTrials.gov study NCT03587103. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
Calcium Channel Blockade in Primary Aldosteronism
ClinicalTrials.gov study NCT04179019. IPD Sharing: YES. Countries: 1. Publications: 0.
Interactions Between HIV Protease Inhibitors and Calcium Channel Blockers
ClinicalTrials.gov study NCT00039975. IPD Sharing: Not stated. Countries: 1. Publications: 5.
Use of a Calcium Channel Blocker to Prevent Premature Luteinizing Hormone Surges in Infertility Patients
ClinicalTrials.gov study NCT01551368. IPD Sharing: Not stated. Countries: 1. Publications: 1.
The Japan-Combined Treatment With Olmesartan and a Calcium Channel Blocker Versus Olmesartan and Diuretics Randomized Efficacy Study (J-CORE)
ClinicalTrials.gov study NCT00607035. IPD Sharing: Not stated. Countries: 1. Publications: 3.
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Allen Brain Atlas
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