RGD Reference Report - Rapid protein kinase C-dependent reduction of rat skeletal muscle voltage-gated sodium channels by ciliary neurotrophic factor. - Rat Genome Database

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Rapid protein kinase C-dependent reduction of rat skeletal muscle voltage-gated sodium channels by ciliary neurotrophic factor.

Authors: Talon, S  Giroux-Metges, MA  Pennec, JP  Guillet, C  Gascan, H  Gioux, M 
Citation: Talon S, etal., J Physiol. 2005 Jun 15;565(Pt 3):827-41. Epub 2005 Apr 14.
RGD ID: 1626125
Pubmed: PMID:15831538   (View Abstract at PubMed)
PMCID: PMC1464552   (View Article at PubMed Central)
DOI: DOI:10.1113/jphysiol.2005.084681   (Journal Full-text)

The ciliary neurotrophic factor (CNTF), known to exert long-term myotrophic effects, has not yet been shown to induce a rapid biological response in skeletal muscles. The present in vitro study gives rise to the possibility that CNTF could affect the sodium channel activity implied in the triggering of muscle fibre contraction. Therefore, we investigated the effects of an external CNTF application on macroscopic sodium current (I(Na)) in rat native fast-twitch skeletal muscle (flexor digitorum brevis, FDB) by using a cell-attached patch-clamp technique. The I(Na) peak amplitude measured at a depolarizing pulse from -100 to -10 mV is rapidly reduced in a time- and dose-dependent manner by CNTF (0.01-20 ng ml(-1)). The maximal decrease is 25% after 10 min incubation in 2 ng ml(-1) CNTF. There was no alteration in activation or inactivation kinetics, or in activation curves constructed from current-voltage relationships in the presence of CNTF. In contrast, the relative I(Na) inhibition induced by CNTF is accompanied by a hyperpolarizing shift in the midpoint of the inactivation curves: -6 and -10 mV for the steady-state fast and slow inactivation, respectively. Furthermore, CNTF induces a 5 mV hyperpolarization of the resting membrane potential of the fibres. The effects of CNTF are similar to those of 1-oleoyl-2-acetyl-sn-glycerol (OAG), a protein kinase C (PKC) activator, when no effect is observed in the presence of chelerythrine, a PKC inhibitor. These results suggest that, in skeletal muscle, CNTF can rapidly decrease sodium currents by altering inactivation gating, probably through an intracellular PKC-dependent mechanism that could lead to decreased membrane excitability. The present study contributes to a better understanding of the physiological role of endogenous CNTF.



Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
CntfRatmembrane hyperpolarization  IDA in fast-twitch flexor digitorum brevis muscle fibersRGD 
CntfRatpositive regulation of cell population proliferation  IDA Ba/F3 cells expressing Cntf receptorsRGD 
CntfRatregulation of resting membrane potential  IDA in fast-twitch flexor digitorum brevis muscle fibersRGD 

Objects Annotated

Genes (Rattus norvegicus)
Cntf  (ciliary neurotrophic factor)


Additional Information