NaV1.7 and pain: contribution of peripheral nerves
| Autor: | Alina Vyshnevska, Christian Weidner, Jürgen Wittmann, Peter W. Reeh, Ohad Sharon, Roberto De Col, Mohammed A. Nassar, Richard W. Carr, Tal Hoffmann |
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| Rok vydání: | 2017 |
| Předmět: |
Pain Threshold
0301 basic medicine medicine.medical_specialty Sensory Receptor Cells Calcitonin Gene-Related Peptide Central nervous system Action Potentials Pain Mice Transgenic Sensory system Stimulation Nerve fiber 03 medical and health sciences 0302 clinical medicine Ganglia Spinal Physical Stimulation Internal medicine Animals Medicine Pain Measurement Nerve Fibers Unmyelinated business.industry Sodium channel NAV1.7 Voltage-Gated Sodium Channel Mice Inbred C57BL Saphenous nerve Disease Models Animal 030104 developmental biology Anesthesiology and Pain Medicine Endocrinology Rheobase medicine.anatomical_structure Neurology Mutation Mechanosensitive channels Neurology (clinical) business 030217 neurology & neurosurgery |
| Zdroj: | Pain. 159:496-506 |
| ISSN: | 1872-6623 0304-3959 |
| Popis: | The sodium channel NaV1.7 contributes to action potential (AP) generation and propagation. Loss-of-function mutations in patients lead to congenital indifference to pain, though it remains unclear where on the way from sensory terminals to central nervous system the signalling is disrupted. We confirm that conditional deletion of NaV1.7 in advillin-expressing sensory neurons leads to impaired heat and mechanical nociception in behavioural tests. With single-fiber recordings from isolated skin, we found (1) a significantly lower prevalence of heat responsiveness to normally mechanosensitive C-fibers, although (2) the rare heat responses seemed quite vigorous, and (3) heat-induced calcitonin gene-related peptide release was normal. In biophysical respects, although electrical excitability, rheobase, and chronaxy were normal, (4) axonal conduction velocity was 20% slower than in congenic wild-type mice (5) and when challenged with double pulses ( |
| Databáze: | OpenAIRE |
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