QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (16) Citing Articles via Google Scholar Google Scholar Articles by Tsang, C. W. Articles by Charlton, M. P. Search for Related Content PubMed PubMed Citation Articles by Tsang, C. W. Articles by Charlton, M. P. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB CALCIUM COMPOUNDS CALCIUM, ELEMENTAL SODIUM TETRODOTOXIN

 Previous Article  |  Next Article 

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

-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

-Latrotoxin (-LTX) is a neurotoxin that accelerates spontaneous exocytosis independently of extracellular Ca²⁺. Although -LTX increases spontaneous transmitter release at synapses, the mechanism is unknown. We tested the hypothesis that -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 -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 -LTX. The Ca²⁺ source is likely to be mitochondria, because the effects on Ca²⁺ mobilization of CCCP (which depletes mitochondrial Ca²⁺) and of -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 -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 -LTX on transmitter release, these increases do not appear to be necessary. The results show that investigations of Ca²⁺-independent -LTX mechanisms or uses of -LTX to probe exocytosis mechanisms would be complicated by the release of intracellular Ca²⁺, which itself can trigger exocytosis.

Key words: -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:

				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]

				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]

				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]

				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]

				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]

				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