J Physiol Editor in Chief
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Physiol Vol 298 pp 251-269
Copyright © 1980 by The Physiological Society
This Article
Right arrow Full Text (PDF)
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kuba, K
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kuba, K

Release of calcium ions linked to the activation of potassium conductance in a caffeine-treated sympathetic neurone.

K Kuba

1. The mechanism of spontaneous and rhythmic hyperpolarizations which occur in bullfrog sympathetic ganglion cells under the effect of caffeine (2--10 mM) were further analysed. 2. Intracellular injection of EGTA blocked generation of caffeine hyperpolarizations (C-hyperpolarizations): this confirmed the previous conclusion (Kuba & Nishi, 1976) that these hyperpolarizations are caused by rhythmic increases in the K+ conductance (GK) of the membrane as a result of rises in free intracellular Ca2+. 3. The amplitude and duration of a C-hyperpolarization induced by an action potential was a function of the time since the previous one; the longer the interval, greater the area. 4. The relationship between the product of the amplitude and duration of a C-hyperpolarization and the preceding interval depended on external Ca2+; when this was low the relationship shifted, so as to indicate an involvement of a Ca2+ accumulating process in the generation mechanism of C-hyperpolarizations. 5. A rapid lowering of temperature triggered the generation of a C-hyperpolarization before appearance of a rhythmic one. There seemed to be no threshold temperature for the effect of such a cold shock; cooling from any temperature within a certain range (10--25 degrees C) by more than a few degrees was effective. 6. The rapid cooling effect was observed even in a Ca2+-free Mg2+ solution. 7. Dantrolene Na increased the interval between rhythmic C-hyperpolarizations or blocked them, but affected less those triggered by an action potential or cold shock. 8. Intracellular injection of Ca2+ triggered the generation of a C-hyperpolarization before the appearance of a rhythmic one. 9. The latency of the generation of an action potential-evoked C-hyperpolarization was dependent on the preceding interval; the shorter the interval, the longer the latency. There was a refractory period for induction of an action potential-induced C-hyperpolarization. 10. The interval between rhythmic C-hyperpolarizations was increased by a small or moderate membrane hyperpolarization (5--20 mV) and decreased by a larger hyperpolarization; the refractory period of an action potential-induced C-hyperpolarization was similarly increased and then decreased by progressive membrane hyperpolarization. 11. These results suggest that rhythmic increases in the GK under the effect of caffeine are due to oscillations of the intracellular Ca2+ concentration and that there may be Ca storage sites in the bullfrog sympathetic ganglion cell which are comparable to the sarcoplasmic reticulum in the skeletal muscle fibre.




This article has been cited by other articles:


Home page
J. Physiol.Home page
T. Akita and K. Kuba
Ca2+-dependent inactivation of Ca2+-induced Ca2+ release in bullfrog sympathetic neurons
J. Physiol., July 15, 2008; 586(14): 3365 - 3384.
[Abstract] [Full Text] [PDF]


Home page
J. Neurophysiol.Home page
J. G. Jackson and S. A. Thayer
Mitochondrial Modulation of Ca2+-Induced Ca2+-Release in Rat Sensory Neurons
J Neurophysiol, September 1, 2006; 96(3): 1093 - 1104.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
S. L. Mironov, M. V. Ivannikov, and M. Johansson
[Ca2+]i Signaling between Mitochondria and Endoplasmic Reticulum in Neurons Is Regulated by Microtubules: FROM MITOCHONDRIAL PERMEABILITY TRANSITION PORE TO Ca2+-INDUCED Ca2+ RELEASE
J. Biol. Chem., January 7, 2005; 280(1): 715 - 721.
[Abstract] [Full Text] [PDF]


Home page
Physiol. Rev.Home page
A. Verkhratsky
Physiology and Pathophysiology of the Calcium Store in the Endoplasmic Reticulum of Neurons
Physiol Rev, January 1, 2005; 85(1): 201 - 279.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
C. A. Parada, G. G. Vivancos, C. H. Tambeli, F. de Queiroz Cunha, and S. H. Ferreira
Activation of presynaptic NMDA receptors coupled to NaV1.8-resistant sodium channel C-fibers causes retrograde mechanical nociceptor sensitization
PNAS, March 4, 2003; 100(5): 2923 - 2928.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
H. Yoshida, Y. Tsunoda, and C. Owyang
Diazepam-binding inhibitor33-50 elicits Ca2+ oscillation and CCK secretion in STC-1 cells via L-type Ca2+ channels
Am J Physiol Gastrointest Liver Physiol, March 1, 1999; 276(3): G694 - G702.
[Abstract] [Full Text] [PDF]


Home page
J. Neurosci.Home page
Y. M. Usachev and S. A. Thayer
All-or-None Ca2+ Release from Intracellular Stores Triggered by Ca2+ Influx through Voltage-Gated Ca2+ Channels in Rat Sensory Neurons
J. Neurosci., October 1, 1997; 17(19): 7404 - 7414.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1980 The Physiological Society.