M
Michael T. Nelson
Researcher at University of Virginia Health System
Publications - 16
Citations - 1633
Michael T. Nelson is an academic researcher from University of Virginia Health System. The author has contributed to research in topics: Voltage-dependent calcium channel & T-type calcium channel. The author has an hindex of 13, co-authored 16 publications receiving 1493 citations. Previous affiliations of Michael T. Nelson include University of Virginia.
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Journal ArticleDOI
Cell-Specific Alterations of T-Type Calcium Current in Painful Diabetic Neuropathy Enhance Excitability of Sensory Neurons
Miljen M. Jagodic,Sriyani Pathirathna,Michael T. Nelson,Stefani Mancuso,Pavle M. Joksovic,Ethan R Rosenberg,Douglas A. Bayliss,Vesna Jevtovic-Todorovic,Slobodan M. Todorovic +8 more
TL;DR: It is found that, in parallel with the development of diabetes-induced pain, T-type current density increased by twofold in medium-size cells from L4–L5 dorsal root ganglia (DRG) with a depolarizing shift in steady-state inactivation, and increased cellular excitability manifested as a lower threshold for burst firing in diabetic than in control cells.
Journal ArticleDOI
Upregulation of the T-type calcium current in small rat sensory neurons after chronic constrictive injury of the sciatic nerve.
Miljen M. Jagodic,Sriyani Pathirathna,Pavle M. Joksovic,Woo Yong Lee,Michael T. Nelson,Ajit K. Naik,Peihan Su,Vesna Jevtovic-Todorovic,Slobodan M. Todorovic +8 more
TL;DR: The finding that T-type currents are upregulated in a CCI model of peripheral neuropathy and earlier pharmacological and molecular studies suggest that T -type channels may be potentially useful therapeutic targets for the treatment of neuropathic pain associated with partial mechanical injury to the sciatic nerve.
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The Endogenous Redox Agent L-Cysteine Induces T-Type Ca2+ Channel-Dependent Sensitization of a Novel Subpopulation of Rat Peripheral Nociceptors
TL;DR: It is demonstrated that the endogenous reducing agent l-cysteine lowers the threshold for nociceptor excitability and induces burst firing by increasing the amplitude of T-type currents and shifting the gating parameters ofT-type channels.
Journal ArticleDOI
In vivo silencing of the CaV3.2 T-type calcium channels in sensory neurons alleviates hyperalgesia in rats with streptozocin-induced diabetic neuropathy
Richard B. Messinger,Ajit K. Naik,Miljen M. Jagodic,Michael T. Nelson,Woo Yong Lee,Woo Yong Lee,Won Joo Choe,Won Joo Choe,Peihan Orestes,Janelle R. Latham,Slobodan M. Todorovic,Vesna Jevtovic-Todorovic +11 more
TL;DR: Treatment of diabetic rats with daily insulin injections reversed T‐current alterations in DRG neurons in parallel with reversal of thermal and mechanical hypersensitivities in vivo, confirming that CaV3.2 T‐channels, important signal amplifiers in peripheral sensory neurons, may contribute to the cellular hyperexcitability that ultimately leads to the development of painful PDN.
Journal ArticleDOI
Reducing Agents Sensitize C-Type Nociceptors by Relieving High-Affinity Zinc Inhibition of T-Type Calcium Channels
Michael T. Nelson,Jiwan Woo,Ho-Won Kang,Iuliia Vitko,Paula Q. Barrett,Edward Perez-Reyes,Jung-Ha Lee,Hee-Sup Shin,Slobodan M. Todorovic +8 more
TL;DR: It is demonstrated that reducing agents as well as endogenous metal chelators sensitize C-type dorsal root ganglion nociceptors by chelating Zn2+ ions off specific extracellular histidine residues on Cav3.2 T-channels, thus relieving tonic channel inhibition, enhancing Cav3-2 currents, and lowering the threshold for nocICEptor excitability in vitro and in vivo.