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Title of Journal: Pflugers Arch Eur J Physiol

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Abbravation: Pflügers Archiv

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Springer-Verlag

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10.1007/s10773-012-1273-9

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1432-2013

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Alterations in calcium homeostasis reduce membrane

Authors: Juliet A UsherSmith Wei Xu James A Fraser Christopher LH Huang
Publish Date: 2006/09/06
Volume: 453, Issue: 2, Pages: 211-221
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Abstract

The effects of alterations in intracellular calcium homeostasis on surface membrane excitability were investigated in resting Rana temporaria sartorius muscle This was prompted by initial results from a fatiguing stimulation protocol study that demonstrated a fibre subpopulation in which action potential generation in response to a standard 15 V electrical stimulus failed despite mean membrane potentials E m −69±23 mV n=14 compatible with spike firing in a control set of quiescent muscle fibres Intracellular microelectrode recordings showed a similar reversible loss of excitability attributable to an increased threshold despite only small 71±18 mV positive changes in E m after approximately 60min exposures to nominally 0 Ca2+ Ringer solutions in which Ca2+ was replaced by Mg2+ This effect was not reproduced by addition of Mg2+ to the Ringer solution and persisted under conditions of Cl− deprivation The effects of three pharmacological agents cyclopiazonic acid CPA caffeine and 4chloromcresol 4CmC each known to deplete store Ca2+ and increase cytosolic Ca2+ through contrasting mechanisms without influencing E m were then investigated All three agents produced a more rapid but nevertheless still reversible loss of membrane excitability than in 0 Ca2+ Ringer solution alone This reduction in membrane excitability persisted in fibres studied in solutions containing a normal Ca2+ following prior depletion of store Ca2+ using CPA and 4CmCcontaining solutions These novel findings suggest that sarcoplasmic reticulum Ca2+ content profoundly influences surface membrane excitability thereby providing a potential mechanism by which spike firing fails in wellpolarised fibres during fatigueWe thank Paul Frost for skilled assistance CLHH thanks the Medical Research Council the Wellcome Trust and the British Heart Foundation for generous support JAUS thanks Astra Zeneca and acknowledges additional support from the James Baird Fund JAF thanks Gonville and Caius College for a research fellowship

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