J Physiol Society Meetings
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Physiol Vol 248, Issue 2 pp 285-306
Copyright © 1975 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 Alnaes, E
Right arrow Articles by Rahamimoff, R
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Alnaes, E
Right arrow Articles by Rahamimoff, R

On the role of mitochondria in transmitter release from motor nerve terminals.

 E Alnaes and R Rahamimoff

1. The changes in transmitter release produced by mitochondrial inhibitors has been studied at the frog neuromuscular junction using conventional electrophysiological techniques for stimulation and intracellular recording. 2. Inhibitors of the electron transport chain and inhibitors of oxidative phosphorylation produce an increase in the frequency of appearance of the miniature end-plate potentials. This increase in frequency is observed also in calcium-free media. Mitochondrial inhibitors also augment the amount of transmitter liberated by a nerve impulse. 3. Ruthenium red, which is an inhibitor of calcium uptake by mitochondria, increases the spontaneous transmitter release but decreases the quantal content. The latter effect of Ruthenium red is antagonized by calcium. 4. The mitochondrial content of the motor nerve terminals is, on the average, 6.59%. 5. The experimental results are explained on the hypothesis that spontaneous release of transmitter reflects the resting level of intracellular free calcium and the evoked release reflects the sum of the resting calcium and the calcium brought in by the action potential. The mitochondria play a role in transmitter release by participating in the regulation of the intracellular free Ca.




This article has been cited by other articles:


Home page
 Mol. Biol. CellHome page
C. W. Lee and H. B. Peng
The Function of Mitochondria in Presynaptic Development at the Neuromuscular Junction
Mol. Biol. Cell, January 1, 2008; 19(1): 150 - 158.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
E.-L. Belair, J. Vallee, and R. Robitaille
Long-term in vivo modulation of synaptic efficacy at the neuromuscular junction of Rana pipiens frogs
J. Physiol., November 15, 2005; 569(1): 163 - 178.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurophysiol.Home page
J. D. Talbot, G. David, and E. F. Barrett
Inhibition of Mitochondrial Ca2+ Uptake Affects Phasic Release From Motor Terminals Differently Depending on External [Ca2+]
J Neurophysiol, July 1, 2003; 90(1): 491 - 502.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurophysiol.Home page
K. Medler and E. L. Gleason
Mitochondrial Ca2+ Buffering Regulates Synaptic Transmission Between Retinal Amacrine Cells
J Neurophysiol, March 1, 2002; 87(3): 1426 - 1439.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
N. Zhong, V. Beaumont, and R. S. Zucker
Roles for Mitochondrial and Reverse Mode Na+/Ca2+ Exchange and the Plasmalemma Ca2+ ATPase in Post-Tetanic Potentiation at Crayfish Neuromuscular Junctions
J. Neurosci., December 15, 2001; 21(24): 9598 - 9607.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
C. W. Tsang, D. B. Elrick, and M. P. Charlton
alpha -Latrotoxin Releases Calcium in Frog Motor Nerve Terminals
J. Neurosci., December 1, 2000; 20(23): 8685 - 8692.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
D. R. Giovannucci, M. D. Hlubek, and E. L. Stuenkel
Mitochondria Regulate the Ca2+-Exocytosis Relationship of Bovine Adrenal Chromaffin Cells
J. Neurosci., November 1, 1999; 19(21): 9261 - 9270.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
G. David
Mitochondrial Clearance of Cytosolic Ca2+ in Stimulated Lizard Motor Nerve Terminals Proceeds without Progressive Elevation of Mitochondrial Matrix [Ca2+]
J. Neurosci., September 1, 1999; 19(17): 7495 - 7506.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
A. Meir, S. Ginsburg, A. Butkevich, S. G. Kachalsky, I. Kaiserman, R. Ahdut, S. Demirgoren, and R. Rahamimoff
Ion Channels in Presynaptic Nerve Terminals and Control of Transmitter Release
Physiol Rev, July 1, 1999; 79(3): 1019 - 1088.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurophysiol.Home page
M. Sciancalepore, J. Gyori, and E. Cherubini
Facilitation of Miniature GABAergic Currents by Ruthenium Red in Neonatal Rat Hippocampal Neurons
J Neurophysiol, November 1, 1998; 80(5): 2316 - 2322.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
G. M. G. Shepherd and K. M. Harris
Three-Dimensional Structure and Composition of CA3right-arrowCA1 Axons in Rat Hippocampal Slices: Implications for Presynaptic Connectivity and Compartmentalization
J. Neurosci., October 15, 1998; 18(20): 8300 - 8310.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurophysiol.Home page
P. V. Nguyen, L. Marin, and H. L. Atwood
Synaptic Physiology and Mitochondrial Function in Crayfish Tonic and Phasic Motor Neurons
J Neurophysiol, July 1, 1997; 78(1): 281 - 294.
[Abstract] [Full Text] [PDF]

Home page
 Cold Spring Harb Symp Quant BiolHome page
R. Rahamimoff, S. D. Erulkar, E. Alnaes, H. Meiri, S. Rotshenker, and H. Rahamimoff
Modulation of Transmitter Release by Calcium Ions and Nerve Impulses
Cold Spring Harb Symp Quant Biol, January 1, 1976; 40(0): 107 - 116.
[Abstract] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1975 The Physiological Society.