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


     

Physiology in Press

First published online on February 14, 2003.
 Copyright © 2003 by The Physiological Society
This Article
Right arrow Full Text (Rapid PDF)
Right arrow All Versions of this Article:
548/2/425    most recent
2002.035196v1
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 David, G.
Right arrow Articles by Barrett, E. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by David, G.
Right arrow Articles by Barrett, E. F.

Received October 30, 2002
Accepted after revision January 21, 2003

Mitochondrial Ca2+ uptake prevents desynchronization of quantal release and minimizes depletion during repetitive stimulation of mouse motor nerve terminals

G. David1* and Ellen F. Barrett2

1 Department of Physiology and Biophysics R-430, University of Miami School of Medicine, PO Box 016430, Miami, FL 33101, USA
2 Department of Physiology and Biophysics, University of Miami School of Medicine, Miami, FL, USA

* To whom correspondence should be addressed. E-mail: gdavid{at}newssun.med.miami.edu.

We investigated how inhibition of mitochondrial Ca2+ uptake affects transmitter release from mouse motor terminals during brief trains of action potentials (500 at 50 Hz) in physiological bath [Ca2+]. When mitochondrial Ca2+ uptake was inhibited by depolarizing mitochondria with antimycin A1 or carbonyl cyanide m-chlorophenyl-hydrazone, the stimulation-induced increase in cytosolic [Ca2+] was greater (> 10 µM, compared to <= 1µM in control solution), the quantal content of the endplate potential (EPP) depressed more rapidly (~84 % depression compared to ~8 % in controls), and asynchronous release during the stimulus train reached higher frequencies (peak rates of ~6000 s-1 compared to ~75 s-1 in controls). These effects of mitochondrial depolarization were not accompanied by a significant change in EPP quantal content or the rate of asynchronous release during 1 Hz stimulation, and were not seen in oligomycin, which blocks mitochondrial ATP synthesis without depolarizing mitochondria. Inhibition of endoplasmic reticular Ca2+ uptake with cyclopiazonic acid also had little effect on stimulation-induced changes in cytosolic [Ca2+] or EPP amplitude. We hypothesize that the high rate of asynchronous release evoked by stimulation during mitochondrial depolarization was produced by the elevation of cytosolic [Ca2+], and contributed to the accelerated depression of phasic release by reducing the availability of releasable vesicles. During mitochondrial depolarization, the post-tetanic potentiation of the EPP observed under control conditions was replaced by a post-tetanic depression with a slow time course of recovery. Thus, mitochondrial Ca2+ uptake is essential for sustaining phasic release, and thus neuromuscular transmission, during and following tetanic stimulation.




This article has been cited by other articles:


Home page
 J. Neurosci.Home page
K. J. Iremonger and J. S. Bains
Integration of Asynchronously Released Quanta Prolongs the Postsynaptic Spike Window
J. Neurosci., June 20, 2007; 27(25): 6684 - 6691.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
M. Avissar, A. C. Furman, J. C. Saunders, and T. D. Parsons
Adaptation Reduces Spike-Count Reliability, But Not Spike-Timing Precision, of Auditory Nerve Responses
J. Neurosci., June 13, 2007; 27(24): 6461 - 6472.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
L. Nunez, L. Senovilla, S. Sanz-Blasco, P. Chamero, M. T. Alonso, C. Villalobos, and J. Garcia-Sancho
Bioluminescence imaging of mitochondrial Ca2+ dynamics in soma and neurites of individual adult mouse sympathetic neurons
J. Physiol., April 15, 2007; 580(2): 385 - 395.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
O. Kann and R. Kovacs
Mitochondria and neuronal activity
Am J Physiol Cell Physiol, February 1, 2007; 292(2): C641 - C657.
[Abstract] [Full Text] [PDF]

Home page
 NeuroscientistHome page
C. V. Ly and P. Verstreken
Mitochondria at the Synapse
Neuroscientist, August 1, 2006; 12(4): 291 - 299.
[Abstract] [PDF]

Home page
 J. Physiol.Home page
L. E. Garcia-Chacon, K. T. Nguyen, G. David, and E. F. Barrett
Extrusion of Ca2+ from mouse motor terminal mitochondria via a Na+-Ca2+ exchanger increases post-tetanic evoked release
J. Physiol., August 1, 2006; 574(3): 663 - 675.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
D. T. W. Chang, A. S. Honick, and I. J. Reynolds
Mitochondrial trafficking to synapses in cultured primary cortical neurons.
J. Neurosci., June 28, 2006; 26(26): 7035 - 7045.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
M. R. Pagani, R. C. Reisin, and O. D. Uchitel
Calcium signaling pathways mediating synaptic potentiation triggered by amyotrophic lateral sclerosis IgG in motor nerve terminals.
J. Neurosci., March 8, 2006; 26(10): 2661 - 2672.
[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 HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Copyright © 2003 The Physiological Society.