Calcium‐induced calcium release in rat sensory neurons.

Calcium‐induced calcium release in rat sensory neurons. 1. In isolated dorsal root ganglion cells (DRG neurons), changes in the concentration of global cytosolic Ca2+ (delta (Ca2+)c) were measured by the fluorescence of K5‐indo‐1. Depolarizations from ‐60 to 0 mV (500 ms) and Ca2+ influx through Ca2+ channels (ICa) increased (Ca2+)c by 480 +/‐ 113 nM, the peak occurring 542 +/‐ 76 ms (mean +/‐ S.E.M.) after repolarization. 2. Ryanodine (10 microM) reduced depolarization‐induced delta (Ca2+)c by up to 80% and blocked delta (Ca2+)c induced by 20 mM caffeine. 3. Peak delta (Ca2+)c and peak ICa followed a similar bell‐shaped voltage dependence. Removal of extracellular Ca2+ abolished depolarization‐induced delta (Ca2+)c; its elevation from 2 to 8 mM increased peak ICa by 30% and delta (Ca2+)c by 108%. 4. Ca2+ influx at 0 mV was graded by pulse durations between 20 and 500 ms. Up to 200 ms, delta (Ca2+)c increased linearly with Ca2+ influx. Depolarizations longer than 200 ms induced a supralinear increase in delta (Ca2+)c that was abolished by caffeine (20 mM). 5. The supralinear increase in delta (Ca2+)c and the caffeine‐induced delta (Ca2+)c were measured only in thirteen of nineteen DRG neurons; in the other six of nineteen cells both properties were absent. The results suggest that Ca(2+)‐induced Ca2+ release (CICR) is expressed differently in different populations of DRG neurons. 6. A single action potential did not significantly increase (Ca2+)c. Trains of stimuli (20 Hz) induced delta (Ca2+)c that linearly increased with the number of action potentials. Delta (Ca2+)c due to 100 action potentials had a significant ryanodine‐sensitive component. 7. It is discussed that CICR can contribute to the depolarization‐induced (Ca2+)c, provided the Ca2+ influx lasts for a certain minimum period of time. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Physiology Wiley

Calcium‐induced calcium release in rat sensory neurons.

The Journal of Physiology, Volume 489 (3) – Dec 15, 1995

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Publisher
Wiley
Copyright
© 2014 The Physiological Society
ISSN
0022-3751
eISSN
1469-7793
D.O.I.
10.1113/jphysiol.1995.sp021078
Publisher site
See Article on Publisher Site

Abstract

1. In isolated dorsal root ganglion cells (DRG neurons), changes in the concentration of global cytosolic Ca2+ (delta (Ca2+)c) were measured by the fluorescence of K5‐indo‐1. Depolarizations from ‐60 to 0 mV (500 ms) and Ca2+ influx through Ca2+ channels (ICa) increased (Ca2+)c by 480 +/‐ 113 nM, the peak occurring 542 +/‐ 76 ms (mean +/‐ S.E.M.) after repolarization. 2. Ryanodine (10 microM) reduced depolarization‐induced delta (Ca2+)c by up to 80% and blocked delta (Ca2+)c induced by 20 mM caffeine. 3. Peak delta (Ca2+)c and peak ICa followed a similar bell‐shaped voltage dependence. Removal of extracellular Ca2+ abolished depolarization‐induced delta (Ca2+)c; its elevation from 2 to 8 mM increased peak ICa by 30% and delta (Ca2+)c by 108%. 4. Ca2+ influx at 0 mV was graded by pulse durations between 20 and 500 ms. Up to 200 ms, delta (Ca2+)c increased linearly with Ca2+ influx. Depolarizations longer than 200 ms induced a supralinear increase in delta (Ca2+)c that was abolished by caffeine (20 mM). 5. The supralinear increase in delta (Ca2+)c and the caffeine‐induced delta (Ca2+)c were measured only in thirteen of nineteen DRG neurons; in the other six of nineteen cells both properties were absent. The results suggest that Ca(2+)‐induced Ca2+ release (CICR) is expressed differently in different populations of DRG neurons. 6. A single action potential did not significantly increase (Ca2+)c. Trains of stimuli (20 Hz) induced delta (Ca2+)c that linearly increased with the number of action potentials. Delta (Ca2+)c due to 100 action potentials had a significant ryanodine‐sensitive component. 7. It is discussed that CICR can contribute to the depolarization‐induced (Ca2+)c, provided the Ca2+ influx lasts for a certain minimum period of time.

Journal

The Journal of PhysiologyWiley

Published: Dec 15, 1995

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