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J. Biol. Chem., Vol. 275, Issue 48, 37488-37495, December 1, 2000

This Article Full Text Full Text (PDF) All Versions of this Article: 275/48/37488    most recent M007388200v1 Submit a Letter to Editor 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 PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Alés, E. Articles by López, M. G. Search for Related Content PubMed PubMed Citation Articles by Alés, E. Articles by López, M. G. Social Bookmarking                      What's this?

The Sea Anemone Toxin Bc2 Induces Continuous or Transient Exocytosis, in the Presence of Sustained Levels of High Cytosolic Ca²⁺ in Chromaffin Cells^*

Eva Alés^§, Nelson H. Gabilan^¶, María F. Cano-Abad^**, Antonio G. García, and Manuela G. López

From the  Instituto de Farmacología Teófilo Hernando, Departamento de Farmacología, Facultad de Medicina, Universidad Autónoma de Madrid, C/Arzobispo Morcillo 4, 28029 Madrid, Spain, the  Servicio de Farmacología Clínica and Instituto de Gerontología, Hospital de la Princesa, C/Diego de León 62, 28006 Madrid, Spain, and the ^¶ Departamento de Bioquímica, Universidade Federal de Santa Catarina, Florianópolis 88049 SC, Brazil

We have isolated and characterized a new excitatory toxin from the venom of the sea anemone Bunodosoma caissarum, named Bc2. We investigated the mechanism of action of the toxin on Ca²⁺-regulated exocytosis in single bovine adrenal chromaffin cells, monitoring simultaneously fura-2 fluorescence measurements and electrochemical recordings using a carbon fiber microelectrode. Bc2 induced quantal release of catecholamines in a calcium-dependent manner. This release was associated with a sustained rise in cytosolic Ca²⁺ and displayed two different patterns of response: a continuous discharge of prolonged duration that changed to a transient burst as the toxin concentration (or incubation time) increased. Continuous secretion was dependent on the activity of native voltage-dependent Ca²⁺ channels and showed a pattern similar to that of -latrotoxin; however, its kinetics adjusted better to that of continuous cell depolarization with high K⁺ concentration. In contrast, transient secretion was independent of Ca²⁺ entry through native voltage-dependent Ca²⁺ channels and showed inhibition of late vesicle fusion that was accompanied by "freezing" of F-actin disassembly. These new features make Bc2 a promising new tool for studying the machinery of neurotransmitter release.

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