Simultaneous recording of intramembrane charge movement components and calcium release in wild-type and S100A1-/- muscle fibres.

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TitleSimultaneous recording of intramembrane charge movement components and calcium release in wild-type and S100A1-/- muscle fibres.
Publication TypeJournal Article
Year of Publication2009
AuthorsProsser, BL, Hernández-Ochoa, EO, Zimmer, DB, Schneider, MF
JournalJ Physiol
Volume587
IssuePt 18
Pagination4543-59
Date Published2009 Sep 15
ISSN1469-7793
KeywordsAnimals, Calcium, Calcium Signaling, Cell Membrane, Cells, Cultured, Ion Channel Gating, Membrane Potentials, Mice, Mice, Inbred C57BL, Mice, Knockout, Muscle Cells, Ryanodine Receptor Calcium Release Channel, S100 Proteins
Abstract

In the preceding paper, we reported that flexor digitorum brevis (FDB) muscle fibres from S100A1 knock-out (KO) mice exhibit a selective suppression of the delayed, steeply voltage-dependent component of intra-membrane charge movement current termed Q(gamma). Here, we use 50 microm of the Ca(2+) indicator fluo-4 in the whole cell patch clamp pipette, in addition to 20 mM EGTA and other constituents included for the charge movement studies, and calculate the SR Ca(2+) release flux from the fluo-4 signals during voltage clamp depolarizations. Ca(2+) release flux is decreased in amplitude by the same fraction at all voltages in fibres from S100A1 KO mice compared to fibres from wild-type (WT) littermates, but unchanged in time course at each pulse membrane potential. There is a strong correlation between the time course and magnitude of release flux and the development of Q(gamma). The decreased Ca(2+) release in KO fibres is likely to account for the suppression of Q(gamma) in these fibres. Consistent with this interpretation, 4-chloro-m-cresol (4-CMC; 100 microm) increases the rate of Ca(2+) release and restores Q(gamma) at intermediate depolarizations in fibres from KO mice, but does not increase Ca(2+) release or restore Q(gamma) at large depolarizations. Our findings are consistent with similar activation kinetics for SR Ca(2+) channels in both WT and KO fibres, but decreased Ca(2+) release in the KO fibres possibly due to shorter SR channel open times. The decreased Ca(2+) release at each voltage is insufficient to activate Q(gamma) in fibres lacking S100A1.

DOI10.1113/jphysiol.2009.177246
Alternate JournalJ. Physiol. (Lond.)
PubMed ID19651766
PubMed Central IDPMC2766656
Grant ListR01 AR055099 / AR / NIAMS NIH HHS / United States
T32 AR007592 / AR / NIAMS NIH HHS / United States