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J Physiol Volume 514, Number 1, 83-99, January 1, 1999
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The Journal of Physiology (1999), 514.1, pp. 83-99
© Copyright 1999 The Physiological Society

Caffeine-induced [Ca2+] oscillations in neurones of frog sympathetic ganglia

Zoltán Cseresnyés, Alexander I. Bustamante and Martin F. Schneider

Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, 108 N. Greene Street, Baltimore, MD 21201, USA


Single cell fluorimetry was used to monitor caffeine-induced oscillations of cytosolic [Ca2+] in frog sympathetic ganglion neurones in 2·0 mM K+ Ringer solution.


[Ca2+] oscillations decreased in frequency and exhibited three different amplitude patterns after the first large peak of [Ca2+]: (a) a series of big oscillations (BOs) of constant large amplitude (300-400 nM), (b) a series of much smaller oscillations (SOs) (40-60 nM), or (c) a series of decaying oscillations (DOs) of rapidly decreasing amplitude.


A model in which the oscillation amplitude was determined by the Ca2+ content of the endoplasmic reticulum (ER) whereas the oscillation frequency was controlled by how rapidly the cytosolic [Ca2+] reached the threshold for Ca2+-induced Ca2+ release (CICR) was able to simulate each observed pattern by varying the level of activity of the ER Ca2+ pump (SERCA), CICR and release-activated Ca2+ transport (RACT). A cumulative, cytosolic Ca2+-dependent inactivation of the plasma membrane (PM) Ca2+ influx or of the Ca2+-sensitive leak coefficient of the ryanodine receptors caused the oscillation frequency to decrease in the model.


Transitions between BOs and SOs and changes in [Ca2+] oscillations caused by ryanodine, thapsigargin, lanthanum and FCCP could also be simulated.


We conclude that RACT, SERCA, CICR and Ca2+-dependent PM Ca2+ influx are major mechanisms underlying [Ca2+] oscillations in these neurones.


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S. I. McDonough, Z. Cseresnyes, and M. F. Schneider
Origin Sites of Calcium Release and Calcium Oscillations in Frog Sympathetic Neurons
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