G W Zamponi
Affiliation: University of Calgary
- Zhang Z, Gadotti V, Chen L, Souza I, Stemkowski P, Zamponi G. Role of Prelimbic GABAergic Circuits in Sensory and Emotional Aspects of Neuropathic Pain. Cell Rep. 2015;12:752-9 pubmed publisher..Our findings thus demonstrate an important role of the prelimbic area in sensory and emotional aspects of pain and identify GABAergic circuits in this region as a potential target for pain therapeutics. ..
- Gadotti V, Bladen C, Zhang F, Chen L, GÃ¼ndÃ¼z M, ÅžimÅŸek R, et al. Analgesic effect of a broad-spectrum dihydropyridine inhibitor of voltage-gated calcium channels. Pflugers Arch. 2015;467:2485-93 pubmed publisher..3 (T-type) and Cav2.2 (N-type) currents. Altogether, our data indicate that broad-spectrum inhibition of multiple calcium channel subtypes can lead to potent analgesia in rodents. ..
- Souza I, Gandini M, Wan M, Zamponi G. Two heterozygous Cav3.2 channel mutations in a pediatric chronic pain patient: recording condition-dependent biophysical effects. Pflugers Arch. 2016;468:635-42 pubmed publisher..Our results show that experimental conditions can be a confounding factor in the biophysical effects of T-type calcium channel mutations found in certain neurological disorders. ..
- Zhang F, Gadotti V, Souza I, Chen L, Zamponi G. BK Potassium Channels Suppress Cavα2δ Subunit Function to Reduce Inflammatory and Neuropathic Pain. Cell Rep. 2018;22:1956-1964 pubmed publisher..Collectively, our data reveal an endogenous ligand of the Cavα2δ subunit with analgesic properties. ..
- Huang J, Zamponi G. Regulation of voltage gated calcium channels by GPCRs and post-translational modification. Curr Opin Pharmacol. 2017;32:1-8 pubmed publisher..Here we focus on select aspects of these regulatory mechanisms and highlight recent developments. ..
- Garcia Caballero A, Gadotti V, Chen L, Zamponi G. A cell-permeant peptide corresponding to the cUBP domain of USP5 reverses inflammatory and neuropathic pain. Mol Pain. 2016;12: pubmed publisher..2 channels. Targeting the interaction of this region with the Cav3.2 channel can be exploited as the basis for therapeutic intervention into inflammatory and neuropathic pain. ..
- Pudukulatham Z, Zhang F, Gadotti V, M Dahoma S, Swami P, Tamboli Y, et al. Synthesis and characterization of a disubstituted piperazine derivative with T-type channel blocking action and analgesic properties. Mol Pain. 2016;12: pubmed publisher..2 channels. Altogether, our data identify a novel T-type calcium channel blocker with tight structure activity relationship (SAR) and relevant in vivo efficacy in inflammatory pain conditions. ..
- Zamponi G, Lewis R, Todorovic S, Arneric S, Snutch T. Role of voltage-gated calcium channels in ascending pain pathways. Brain Res Rev. 2009;60:84-9 pubmed publisher..Here, we provide a brief overview of recent advances in this area, as presented at the Spring Pain Research conference (Grand Cayman, 2008). ..
- Bourinet E, Zamponi G. Block of voltage-gated calcium channels by peptide toxins. Neuropharmacology. 2017;127:109-115 pubmed publisher..This article is part of the Special Issue entitled 'Venom-derived Peptides as Pharmacological Tools.' ..
- Stemkowski P, GarcÃa Caballero A, Gadotti V, M Dahoma S, Huang S, Black S, et al. TRPV1 Nociceptor Activity Initiates USP5/T-type Channel-Mediated Plasticity. Cell Rep. 2016;17:2901-2912 pubmed publisher..2 channel activity. This neuronal-activity-induced USP5 upregulation may underlie a protective, transient sensitization of the pain pathway. ..
- Kim J, Jeong H, Jung D, Yoon H, Kim S, Kim H, et al. Synthesis and biological evaluation of fluoro-substituted 3,4-dihydroquinazoline derivatives for cytotoxic and analgesic effects. Bioorg Med Chem. 2017;25:4656-4664 pubmed publisher..In addition, compound 8g (KCP10067F) was found to partially protect from inflammatory pain via a blockade of Cav3.2 channels. ..
- Proft J, Rzhepetskyy Y, Lazniewska J, Zhang F, Cain S, Snutch T, et al. The Cacna1h mutation in the GAERS model of absence epilepsy enhances T-type Ca2+ currents by altering calnexin-dependent trafficking of Cav3.2 channels. Sci Rep. 2017;7:11513 pubmed publisher..Our study reveals a novel mechanism that controls the expression of T-type channels, and provides a molecular explanation for the enhancement of T-type calcium conductance in GAERS. ..
- Gadotti V, Caballero A, Berger N, Gladding C, Chen L, Pfeifer T, et al. Small organic molecule disruptors of Cav3.2 - USP5 interactions reverse inflammatory and neuropathic pain. Mol Pain. 2015;11:12 pubmed publisher..Overall, our findings provide proof of concept for a new class of analgesics that target T-type channel deubiquitination. ..
- GarcÃa Caballero A, Gadotti V, Stemkowski P, Weiss N, Souza I, Hodgkinson V, et al. The deubiquitinating enzyme USP5 modulates neuropathic and inflammatory pain by enhancing Cav3.2 channel activity. Neuron. 2014;83:1144-58 pubmed publisher..Altogether, our experiments reveal a cell signaling pathway that regulates T-type channel activity and their role in nociceptive signaling. ..
- Simms B, Souza I, Zamponi G. Effect of the Brugada syndrome mutation A39V on calmodulin regulation of Cav1.2 channels. Mol Brain. 2014;7:34 pubmed publisher..Our data indicate that caution must be exercised when interpreting the effects of CaM mutants on ion channel gating. ..
- Simms B, Zamponi G. Neuronal voltage-gated calcium channels: structure, function, and dysfunction. Neuron. 2014;82:24-45 pubmed publisher..This Review discusses salient aspects of voltage-gated calcium channel function, physiology, and pathophysiology. ..
- Zamponi G, Stys P. Role of prions in neuroprotection and neurodegeneration: a mechanism involving glutamate receptors?. Prion. 2009;3:187-9 pubmed..Such is a functional link between NMDA receptors and normal prion protein, and therefore possibly between these receptors and pathological prion isoforms, raises interesting therapeutic possibilities for prion diseases. ..