WWW.JNEUROSCI.ORG
-
The Journal of Neuroscience ScienceCareers.org
 QUICK SEARCH:   [advanced]


     
-


HOME
  |  
SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit an eLetter
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (12)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Tsang, C. W.
Right arrow Articles by Charlton, M. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tsang, C. W.
Right arrow Articles by Charlton, M. P.

 Previous Article  |  Next Article 

The Journal of Neuroscience, December 1, 2000, 20(23):8685-8692

alpha -Latrotoxin Releases Calcium in Frog Motor Nerve Terminals

Christopher W. Tsang, Donald B. Elrick, and Milton P. Charlton

Department of Physiology, University of Toronto, Toronto, Canada M5S 1A8

alpha -Latrotoxin (alpha -LTX) is a neurotoxin that accelerates spontaneous exocytosis independently of extracellular Ca2+. Although alpha -LTX increases spontaneous transmitter release at synapses, the mechanism is unknown. We tested the hypothesis that alpha -LTX causes transmitter release by mobilizing intracellular Ca2+ in frog motor nerve terminals. Transmitter release was measured electrophysiologically and with the vesicle marker FM1-43; presynaptic ion concentration dynamics were measured with fluorescent ion-imaging techniques. We report that alpha -LTX increases transmitter release after release of a physiologically relevant concentration of intracellular Ca2+. Neither the blockade of Ca2+ release nor the depletion of Ca2+ from endoplasmic reticulum affected Ca2+ signals produced by alpha -LTX. The Ca2+ source is likely to be mitochondria, because the effects on Ca2+ mobilization of CCCP (which depletes mitochondrial Ca2+) and of alpha -LTX are mutually occlusive. The release of mitochondrial Ca2+ is partially attributable to an increase in intracellular Na+, suggesting that the mitochondrial Na+/Ca2+ exchanger is activated. Effects of alpha -LTX were not blocked when Ca2+ increases were reduced greatly in saline lacking both Na+ and Ca2+ and by application of intracellular Ca2+ chelators. Therefore, although increases in intracellular Ca2+ may facilitate the effects of alpha -LTX on transmitter release, these increases do not appear to be necessary. The results show that investigations of Ca2+-independent alpha -LTX mechanisms or uses of alpha -LTX to probe exocytosis mechanisms would be complicated by the release of intracellular Ca2+, which itself can trigger exocytosis.

Key words: alpha -latrotoxin; presynaptic toxin; mitochondria; calcium; sodium; exocytosis; frog neuromuscular junction/motor nerve terminal


Copyright © 2000 Society for Neuroscience  0270-6474/00/20238685-08$05.00/0


This article has been cited by other articles:


Home page
J. Biol. Chem.Home page
S. Lajus, P. Vacher, D. Huber, M. Dubois, M.-N. Benassy, Y. Ushkaryov, and J. Lang
{alpha}-Latrotoxin Induces Exocytosis by Inhibition of Voltage-dependent K+ Channels and by Stimulation of L-type Ca2+ Channels via Latrophilin in beta-Cells
J. Biol. Chem., March 3, 2006; 281(9): 5522 - 5531.
[Abstract] [Full Text] [PDF]


Home page
J. Physiol.Home page
A. M Silva, J. Liu-Gentry, A. S Dickey, D. W Barnett, and S. Misler
{alpha}-Latrotoxin increases spontaneous and depolarization-evoked exocytosis from pancreatic islet {beta}-cells
J. Physiol., June 15, 2005; 565(3): 783 - 799.
[Abstract] [Full Text] [PDF]


Home page
J. Cell Biol.Home page
F. Yang, X.-p. He, J. Russell, and B. Lu
Ca2+ influx-independent synaptic potentiation mediated by mitochondrial Na+-Ca2+ exchanger and protein kinase C
J. Cell Biol., November 10, 2003; 163(3): 511 - 523.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
K. E. Volynski, M. Capogna, A. C. Ashton, D. Thomson, E. V. Orlova, C. F. Manser, R. R. Ribchester, and Y. A. Ushkaryov
Mutant {alpha}-Latrotoxin (LTXN4C) Does Not Form Pores and Causes Secretion by Receptor Stimulation: THIS ACTION DOES NOT REQUIRE NEUREXINS
J. Biol. Chem., August 15, 2003; 278(33): 31058 - 31066.
[Abstract] [Full Text] [PDF]


Home page
J. Neurosci.Home page
S. O. Rizzoli and W. J. Betz
Effects of 2-(4-Morpholinyl)-8-Phenyl-4H-1-Benzopyran-4-One on Synaptic Vesicle Cycling at the Frog Neuromuscular Junction
J. Neurosci., December 15, 2002; 22(24): 10680 - 10689.
[Abstract] [Full Text] [PDF]


Home page
J. Neurophysiol.Home page
S. Suzuki, M. Osanai, N. Mitsumoto, T. Akita, K. Narita, H. Kijima, and K. Kuba
Ca2+-Dependent Ca2+ Clearance Via Mitochondrial Uptake and Plasmalemmal Extrusion in Frog Motor Nerve Terminals
J Neurophysiol, April 1, 2002; 87(4): 1816 - 1823.
[Abstract] [Full Text] [PDF]



-

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help

-
Copyright 2008 by Society for Neuroscience ONLINE ISSN: 1529-2401
-