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Verfasst von:Tigerholm, Jenny [VerfasserIn]   i
 Obreja, Otilia [VerfasserIn]   i
 Carr, Richard [VerfasserIn]   i
 Schmelz, Martin [VerfasserIn]   i
Titel:C-fiber recovery cycle supernormality depends on ion concentration and ion channel permeability
Verf.angabe:Jenny Tigerholm, Marcus E. Petersson, Otilia Obreja, Esther Eberhardt, Barbara Namer, Christian Weidner, Angelika Lampert, Richard W. Carr, Martin Schmelz, and Erik Fransén
E-Jahr:2015
Jahr:10 March 2015
Umfang:15 S.
Fussnoten:Gesehen am 12.10.2017
Titel Quelle:Enthalten in: Biophysical journal
Ort Quelle:Cambridge, Mass. : Cell Press, 1960
Jahr Quelle:2015
Band/Heft Quelle:108(2015), 5, Seite 1057-1071
ISSN Quelle:1542-0086
Abstract:Following each action potential, C-fiber nociceptors undergo cyclical changes in excitability, including a period of superexcitability, before recovering their basal excitability state. The increase in superexcitability during this recovery cycle depends upon their immediate firing history of the axon, but also determines the instantaneous firing frequency that encodes pain intensity. To explore the mechanistic underpinnings of the recovery cycle phenomenon a biophysical model of a C-fiber has been developed. The model represents the spatial extent of the axon including its passive properties as well as ion channels and the Na/K-ATPase ion pump. Ionic concentrations were represented inside and outside the membrane. The model was able to replicate the typical transitions in excitability from subnormal to supernormal observed empirically following a conducted action potential. In the model, supernormality depended on the degree of conduction slowing which in turn depends upon the frequency of stimulation, in accordance with experimental findings. In particular, we show that activity-dependent conduction slowing is produced by the accumulation of intraaxonal sodium. We further show that the supernormal phase results from a reduced potassium current Kdr as a result of accumulation of periaxonal potassium in concert with a reduced influx of sodium through Nav1.7 relative to Nav1.8 current. This theoretical prediction was supported by data from an in vitro preparation of small rat dorsal root ganglion somata showing a reduction in the magnitude of tetrodotoxin-sensitive relative to tetrodotoxin -resistant whole cell current. Furthermore, our studies provide support for the role of depolarization in supernormality, as previously suggested, but we suggest that the basic mechanism depends on changes in ionic concentrations inside and outside the axon. The understanding of the mechanisms underlying repetitive discharges in recovery cycles may provide insight into mechanisms of spontaneous activity, which recently has been shown to correlate to a perceived level of pain.
DOI:doi:10.1016/j.bpj.2014.12.034
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.

kostenfrei: Volltext: http://dx.doi.org/10.1016/j.bpj.2014.12.034
 kostenfrei: Volltext: http://www.sciencedirect.com/science/article/pii/S0006349514048127
 DOI: https://doi.org/10.1016/j.bpj.2014.12.034
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:156434178X
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