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Gerald Zamponi

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https://www.readbyqxmd.com/read/29131938/a-crash-course-in-calcium-channels
#1
Gerald W Zamponi
Much progress has been made in understanding the molecular physiology and pharmacology of calcium channels. Recently, there have been tremendous advances in learning about calcium channel structure and function through crystallography and cryo-electron microscopy studies. Here, I will give an overview of our knowledge about calcium channels, and highlight two recent studies that give important insights into calcium channel structure.
November 13, 2017: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/29038242/activity-dependent-facilitation-of-cav1-3-calcium-channels-promotes-kca3-1-activation-in-hippocampal-neurons
#2
Giriraj Sahu, Hadhimulya Asmara, Fang-Xiong Zhang, Gerald W Zamponi, Ray W Turner
CaV1 L-type calcium channels are key to regulating neuronal excitability, with the range of functional roles enhanced by interactions with calmodulin, accessory proteins, or CaMKII that modulate channel activity. In hippocampal pyramidal cells a prominent elevation of CaV1 activity is apparent in late channel openings that can last for seconds following a depolarizing stimulus train. The current study tested the hypothesis that a reported interaction between CaV1.3 channels, the scaffolding protein densin, and CaMKII could generate a facilitation of channel activity that outlasts a depolarizing stimulus...
October 16, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28912545/the-cacna1h-mutation-in-the-gaers-model-of-absence-epilepsy-enhances-t-type-ca-2-currents-by-altering-calnexin-dependent-trafficking-of-cav3-2-channels
#3
Juliane Proft, Yuriy Rzhepetskyy, Joanna Lazniewska, Fang-Xiong Zhang, Stuart M Cain, Terrance P Snutch, Gerald W Zamponi, Norbert Weiss
Low-voltage-activated T-type calcium channels are essential contributors to the functioning of thalamocortical neurons by supporting burst-firing mode of action potentials. Enhanced T-type calcium conductance has been reported in the Genetic Absence Epilepsy Rat from Strasbourg (GAERS) and proposed to be causally related to the overall development of absence seizure activity. Here, we show that calnexin, an endoplasmic reticulum integral membrane protein, interacts with the III-IV linker region of the Cav3...
September 14, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28880874/discovery-and-mode-of-action-of-a-novel-analgesic-%C3%AE-toxin-from-the-african-spider-ceratogyrus-darlingi
#4
Silmara R Sousa, Joshua S Wingerd, Andreas Brust, Christopher Bladen, Lotten Ragnarsson, Volker Herzig, Jennifer R Deuis, Sebastien Dutertre, Irina Vetter, Gerald W Zamponi, Glenn F King, Paul F Alewood, Richard J Lewis
Spider venoms are rich sources of peptidic ion channel modulators with important therapeutical potential. We screened a panel of 60 spider venoms to find modulators of ion channels involved in pain transmission. We isolated, synthesized and pharmacologically characterized Cd1a, a novel peptide from the venom of the spider Ceratogyrus darlingi. Cd1a reversibly paralysed sheep blowflies (PD50 of 1318 pmol/g) and inhibited human Cav2.2 (IC50 2.6 μM) but not Cav1.3 or Cav3.1 (IC50 > 30 μM) in fluorimetric assays...
2017: PloS One
https://www.readbyqxmd.com/read/28800734/a-t-type-channel-calmodulin-complex-triggers-%C3%AE-camkii-activation
#5
Hadhimulya Asmara, Ileana Micu, Arsalan P Rizwan, Giriraj Sahu, Brett A Simms, Fang-Xiong Zhang, Jordan D T Engbers, Peter K Stys, Gerald W Zamponi, Ray W Turner
Calmodulin (CaM) is an important signaling molecule that regulates a vast array of cellular functions by activating second messengers involved in cell function and plasticity. Low voltage-activated calcium channels of the Cav3 family have the important role of mediating low threshold calcium influx, but were not believed to interact with CaM. We find a constitutive association between CaM and the Cav3.1 channel at rest that is lost through an activity-dependent and Cav3.1 calcium-dependent CaM dissociation...
August 11, 2017: Molecular Brain
https://www.readbyqxmd.com/read/28741432/-express-identification-of-interleukin-1-beta-as-a-key-mediator-in-the-upregulation-of-cav3-2-usp5-interactions-in-the-pain-pathway
#6
Patrick L Stemkowski, Agustin Garcia-Caballero, Vinicius M Gadotti, Said M'Dahoma, Lina Chen, Ivana A Souza, Gerald W Zamponi
No abstract text is available yet for this article.
January 2017: Molecular Pain
https://www.readbyqxmd.com/read/28720332/synthesis-and-biological-evaluation-of-fluoro-substituted-3-4-dihydroquinazoline-derivatives-for-cytotoxic-and-analgesic-effects
#7
Jin Han Kim, Hui Rak Jeong, Da Woon Jung, Hong Bin Yoon, Sun Young Kim, Hyoung Ja Kim, Kyung-Tae Lee, Vinicius M Gadotti, Junting Huang, Fang-Xiong Zhang, Gerald W Zamponi, Jae Yeol Lee
As a bioisosteric strategy to overcome the poor metabolic stability of lead compound KYS05090S, a series of new fluoro-substituted 3,4-dihydroquinazoline derivatives was prepared and evaluated for T-type calcium channel (Cav3.2) block, cytotoxic effects and liver microsomal stability. Among them, compound 8h (KCP10068F) containing 4-fluorobenzyl amide and 4-cyclohexylphenyl ring potently blocked Cav3.2 currents (>90% inhibition) at 10μM concentration and exhibited cytotoxic effect (IC50=5.9μM) in A549 non-small cell lung cancer cells that was comparable to KYS05090S...
September 1, 2017: Bioorganic & Medicinal Chemistry
https://www.readbyqxmd.com/read/28664409/surfen-is-a-broad-spectrum-calcium-channel-inhibitor-with-analgesic-properties-in-mouse-models-of-acute-and-chronic-inflammatory-pain
#8
Paula Rivas-Ramirez, Vinicius M Gadotti, Gerald W Zamponi, Norbert Weiss
Multiple voltage-gated calcium channels (VGCCs) contribute to the processing of nociceptive signals in primary afferent fibers. In addition, alteration of calcium channel activity is associated with a number of chronic pain conditions. Therefore, VGCCs have emerged as prime target for the management of either neuropathic or inflammatory pain, and selective calcium channel blockers have been shown to have efficacy in animal models and in the clinic. However, considering that multiple calcium channels contribute pain afferent signaling, broad-spectrum inhibitors of several channel isoforms may offer a net advantage in modulating pain...
June 30, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/28608534/recent-advances-in-the-development-of-t-type-calcium-channel-blockers-for-pain-intervention
#9
REVIEW
Terrance P Snutch, Gerald W Zamponi
Cav 3.2 T-type calcium channels are important regulators of pain signals in the afferent pain pathway, and their activities are dysregulated during various chronic pain states. Therefore, it is reasonable to predict that inhibiting T-type calcium channels in dorsal root ganglion neurons and in the spinal dorsal horn can be targeted for pain relief. This is supported by early pharmacological studies with T-type channel blockers, such as ethosuximide, and by analgesic effects of siRNA depletion of Cav 3.2 channels...
June 13, 2017: British Journal of Pharmacology
https://www.readbyqxmd.com/read/28586339/erratum-blocking-microglial-pannexin-1-channels-alleviates-morphine-withdrawal-in-rodents
#10
Nicole E Burma, Robert P Bonin, Heather Leduc-Pessah, Corey Baimel, Zoe F Cairncross, Michael Mousseau, Jhenkruthi Vijaya Shankara, Patrick L Stemkowski, Dinara Baimoukhametova, Jaideep S Bains, Michael C Antle, Gerald W Zamponi, Catherine M Cahill, Stephanie L Borgland, Yves DeKoninck, Tuan Trang
No abstract text is available yet for this article.
June 6, 2017: Nature Medicine
https://www.readbyqxmd.com/read/28467171/down-regulation-of-t-type-cav3-2-channels-by-hyperpolarization-activated-cyclic-nucleotide-gated-channel-1-hcn1-evidence-of-a-signaling-complex
#11
Jing Fan, Maria A Gandini, Fang-Xiong Zhang, Lina Chen, Ivana A Souza, Gerald W Zamponi
Formation of complexes between ion channels is important for signal processing in the brain. Here we investigate the biochemical and biophysical interactions between HCN1 channels and Cav3.2 T-type channels. We found that HCN1 co-immunoprecipitated with Cav3.2 from lysates of either mouse brain or tsA-201 cells, with the HCN1 N-terminus associating with the Cav3.2 N-terminus. Cav3.2 channel activity appeared to be functionally regulated by HCN1. The expression of HCN1 induced a decrease in Cav3.2 Ba(2+) influx (IBa(2+)) along with altered channel kinetics and a depolarizing shift in activation gating...
September 3, 2017: Channels
https://www.readbyqxmd.com/read/28399450/synthesis-of-new-n3-substituted-dihydropyrimidine-derivatives-as-l-t-type-calcium-channel-blockers
#12
Mohamed Teleb, Fang-Xiong Zhang, Ahmed M Farghaly, Omaima M Aboul Wafa, Frank R Fronczek, Gerald W Zamponi, Hesham Fahmy
Cardiovascular diseases (CVDs) are the main cause of deaths worldwide. Up-to-date, hypertension is the most significant contributing factor to CVDs. Recent clinical studies recommend calcium channel blockers (CCBs) as effective treatment alone or in combination with other medications. Being the most clinically useful CCBs, 1,4-dihydropyridines (DHPs) attracted great interest in improving potency and selectivity. However, the short plasma half-life which may be attributed to the metabolic oxidation to the pyridine-counterparts is considered as a major limitation for this class...
July 7, 2017: European Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/28391067/n-type-ca-2-channels-are-affected-by-full-length-mutant-huntingtin-expression-in-a-mouse-model-of-huntington-s-disease
#13
Flavia R Silva, Artur S Miranda, Rebeca P M Santos, Isabella G Olmo, Gerald W Zamponi, Tomas Dobransky, Jader S Cruz, Luciene B Vieira, Fabiola M Ribeiro
Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by a polyglutamine expansion in the amino-terminal region of the huntingtin (htt) protein. In addition to facilitating neurodegeneration, mutant htt is implicated in HD-related alterations of neurotransmission. Previous data showed that htt can modulate N-type voltage-gated Ca(2+) channels (Cav2.2), which are essential for presynaptic neurotransmitter release. Thus, to elucidate the mechanism underlying mutant htt-mediated alterations in neurotransmission, we investigated how Cav2...
March 18, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/28249172/trpv1-nociceptor-activity-initiates-usp5-t-type-channel-mediated-plasticity
#14
Patrick Stemkowski, Agustin García-Caballero, Vinicius De Maria Gadotti, Said M'Dahoma, Shuo Huang, Stefanie Alice Gertrud Black, Lina Chen, Ivana Assis Souza, Zizhen Zhang, Gerald Werner Zamponi
No abstract text is available yet for this article.
February 28, 2017: Cell Reports
https://www.readbyqxmd.com/read/28230232/carisbamate-blockade-of-t-type-voltage-gated-calcium-channels
#15
Do Young Kim, Fang-Xiong Zhang, Stan T Nakanishi, Timothy Mettler, Ik-Hyun Cho, Younghee Ahn, Florian Hiess, Lina Chen, Patrick G Sullivan, S R Wayne Chen, Gerald W Zamponi, Jong M Rho
OBJECTIVES: Carisbamate (CRS) is a novel monocarbamate compound that possesses antiseizure and neuroprotective properties. However, the mechanisms underlying these actions remain unclear. Here, we tested both direct and indirect effects of CRS on several cellular systems that regulate intracellular calcium concentration [Ca(2+) ]i . METHODS: We used a combination of cellular electrophysiologic techniques, as well as cell viability, Store Overload-Induced Calcium Release (SOICR), and mitochondrial functional assays to determine whether CRS might affect [Ca(2+) ]i levels through actions on the endoplasmic reticulum (ER), mitochondria, and/or T-type voltage-gated Ca(2+) channels...
April 2017: Epilepsia
https://www.readbyqxmd.com/read/28134928/blocking-microglial-pannexin-1-channels-alleviates-morphine-withdrawal-in-rodents
#16
Nicole E Burma, Robert P Bonin, Heather Leduc-Pessah, Corey Baimel, Zoe F Cairncross, Michael Mousseau, Jhenkruthi Vijaya Shankara, Patrick L Stemkowski, Dinara Baimoukhametova, Jaideep S Bains, Michael C Antle, Gerald W Zamponi, Catherine M Cahill, Stephanie L Borgland, Yves De Koninck, Tuan Trang
Opiates are essential for treating pain, but termination of opiate therapy can cause a debilitating withdrawal syndrome in chronic users. To alleviate or avoid the aversive symptoms of withdrawal, many of these individuals continue to use opiates. Withdrawal is therefore a key determinant of opiate use in dependent individuals, yet its underlying mechanisms are poorly understood and effective therapies are lacking. Here, we identify the pannexin-1 (Panx1) channel as a therapeutic target in opiate withdrawal...
March 2017: Nature Medicine
https://www.readbyqxmd.com/read/27974205/trpv1-nociceptor-activity-initiates-usp5-t-type-channel-mediated-plasticity
#17
Patrick Stemkowski, Agustin García-Caballero, Vinicius De Maria Gadotti, Said M'Dahoma, Shuo Huang, Stefanie Alice Gertrud Black, Lina Chen, Ivana Assis Souza, Zizhen Zhang, Gerald Werner Zamponi
Peripheral nerve injury and tissue inflammation result in upregulation of the deubiquitinase USP5, thus causing a dysregulation of T-type calcium channel activity and increased pain sensitivity. Here, we have explored the role of afferent fiber activity in this process. Conditioning stimulation of optogenetically targeted cutaneous TRPV1 expressing nociceptors, but not that of non-nociceptive fibers, resulted in enhanced expression of USP5 in mouse dorsal root ganglia and spinal dorsal horn, along with decreased withdrawal thresholds for thermal and mechanical stimuli that abated after 24 hr...
December 13, 2016: Cell Reports
https://www.readbyqxmd.com/read/27807163/long-term-potentiation-at-the-mossy-fiber-granule-cell-relay-invokes-postsynaptic-second-messenger-regulation-of-kv4-channels
#18
Arsalan P Rizwan, Xiaoqin Zhan, Gerald W Zamponi, Ray W Turner
Mossy fiber afferents to cerebellar granule cells form the primary synaptic relay into cerebellum, providing an ideal site to process signal inputs differentially. Mossy fiber input is known to exhibit a long-term potentiation (LTP) of synaptic efficacy through a combination of presynaptic and postsynaptic mechanisms. However, the specific postsynaptic mechanisms contributing to LTP of mossy fiber input is unknown. The current study tested the hypothesis that LTP induces a change in intrinsic membrane excitability of rat cerebellar granule cells through modification of Kv4 A-type potassium channels...
November 2, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27768908/regulation-of-voltage-gated-calcium-channels-by-gpcrs-and-post-translational-modification
#19
REVIEW
Junting Huang, Gerald W Zamponi
Calcium entry via voltage gated calcium channels mediates a wide range of physiological functions, whereas calcium channel dysregulation has been associated with numerous pathophysiological conditions. There are myriad cell signaling pathways that act on voltage gated calcium channels to fine tune their activities and to regulate their cell surface expression. These regulatory mechanisms include the activation of G protein-coupled receptors and downstream phosphorylation events, and their control over calcium channel trafficking through direct physical interactions...
February 2017: Current Opinion in Pharmacology
https://www.readbyqxmd.com/read/27756538/block-of-voltage-gated-calcium-channels-by-peptide-toxins
#20
Emmanuel Bourinet, Gerald W Zamponi
Venoms from various predatory species, such as fish hunting mollusks scorpions, snakes and arachnids contain a large spectrum of toxins that include blockers of voltage-gated calcium channels. These peptide blockers act by two principal manners - physical occlusion of the pore and prevention of activation gating. Many of the calcium channel-blocking peptides have evolved to tightly occupy their binding pocket on the principal pore forming subunit of the channel, often rendering block poorly reversible. Moreover, several of the best characterized blocking peptides have developed a high degree of channel subtype selectivity...
October 15, 2016: Neuropharmacology
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