Title |
Sea-Anemone Toxin ATX-II Elicits A-Fiber-Dependent Pain and Enhances Resurgent and Persistent Sodium Currents in Large Sensory Neurons
|
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Published in |
Molecular Pain, January 2012
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DOI | 10.1186/1744-8069-8-69 |
Pubmed ID | |
Authors |
Alexandra B Klinger, Mirjam Eberhardt, Andrea S Link, Barbara Namer, Lisa K Kutsche, E Theresa Schuy, Ruth Sittl, Tali Hoffmann, Christian Alzheimer, Tobias Huth, Richard W Carr, Angelika Lampert |
Abstract |
Gain-of-function mutations of the nociceptive voltage-gated sodium channel Nav1.7 lead to inherited pain syndromes, such as paroxysmal extreme pain disorder (PEPD). One characteristic of these mutations is slowed fast-inactivation kinetics, which may give rise to resurgent sodium currents. It is long known that toxins from Anemonia sulcata, such as ATX-II, slow fast inactivation and skin contact for example during diving leads to various symptoms such as pain and itch. Here, we investigated if ATX-II induces resurgent currents in sensory neurons of the dorsal root ganglion (DRGs) and how this may translate into human sensations. |
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