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Verfasst von:Hoffmann, Tal [VerfasserIn]   i
 Carr, Richard [VerfasserIn]   i
Titel:NaV1.7 and pain
Titelzusatz:contribution of peripheral nerves
Verf.angabe:Tal Hoffmann, Ohad Sharon, Jürgen Wittmann, Richard W. Carr, Alina Vyshnevska, Roberto De Col, Mohammed A. Nassar, Peter W. Reeh, Christian Weidner
E-Jahr:2018
Jahr:March 2018
Umfang:11 S.
Fussnoten:Gesehen am 16.06.2020
Titel Quelle:Enthalten in: Pain
Ort Quelle:New York, NY [u.a.] : Lippincott Williams and Wilkins, 1975
Jahr Quelle:2018
Band/Heft Quelle:159(2018), 3, Seite 496-506
ISSN Quelle:1872-6623
Abstract: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 (<100 milliseconds interval), the second AP showed more pronounced latency increase (6). On prolonged electrical stimulation at 2 Hz, (7) activity-dependent slowing of nerve fiber conduction was markedly less, and (8) was less likely to result in conduction failure of the mutant single fibers. Finally, recording of compound APs from the whole saphenous nerve confirmed slower conduction and less activity-dependent slowing as well as the functional absence of a large subpopulation of C-fibers (9) in conditional NaV1.7Adv knockouts. In conclusion, the clear deficits in somatic primary afferent functions shown in our study may be complemented by previously reported synaptic dysfunction and opioidergic inhibition, together accounting for the complete insensitivity to pain in the human mutants lacking NaV1.7.
DOI:doi:10.1097/j.pain.0000000000001119
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1097/j.pain.0000000000001119
 Volltext: https://journals.lww.com/pain/Fulltext/2018/03000/NaV1_7_and_pain__contribution_of_peripheral_nerves.12.aspx
 DOI: https://doi.org/10.1097/j.pain.0000000000001119
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1700664263
Verknüpfungen:→ Zeitschrift

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