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Related Concept Videos

Exocytosis00:51

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Exocytosis is used to release material from cells. Like other bulk transport mechanisms, exocytosis requires energy.
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Exocytosis is a process that releases molecules outside the cell. Like other bulk transport mechanisms, exocytosis requires energy.
Exocytosis is the opposite of endocytosis, which brings molecules inside the cell. Sometimes, the released materials are signaling molecules. For example, neurons typically use exocytosis to release neurotransmitters. Cells also use exocytosis to insert proteins such as ion channels into their cell membranes, secrete proteins for use in the extracellular matrix, or...
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Overview of Secretory Vesicles01:33

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Secretory vesicles, also known as dense core vesicles (DCVs), are membrane-bound vesicles that transport secretory proteins, such as hormones or neurotransmitters. Regulated secretory vesicles transport proteins from the trans-Golgi network to the exterior of the cell. Proteins present in regulated secretory vesicles are required to be rapidly exocytosed in large amounts upon a specific stimulus.
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Fusion of Secretory Vesicles with the Plasma Membrane01:26

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Proteins and neurotransmitters in secretory vesicles can be released from a cell upon vesicle docking, priming, and fusion with the plasma membrane. Vesicles are docked and primed in preparation for the quick exocytosis of their contents in response to a stimulus. The fusion process is mainly carried out by a SNAP Receptor or SNARE complex, consisting of synaptobrevin, syntaxin-1, and SNAP-25.
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SNAREs and Membrane Fusion01:43

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Clathrin-coated vesicles use endocytosis to transport receptors and lysosomal hydrolases from the Golgi to the lysosome in the late secretory pathway. Clathrin-mediated endocytosis was the first described endocytic process, and Clathrin-coated vesicles remain one of the most well-studied transport vesicles. The molecular machinery that generates clathrin-coated vesicles comprises over 50 proteins that precisely coordinate vesicle formation. Cell surface receptors concentrated in indented sites...
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Related Experiment Video

Updated: May 6, 2026

Examination of Synaptic Vesicle Recycling Using FM Dyes During Evoked, Spontaneous, and Miniature Synaptic Activities
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A complexin/synaptotagmin 1 switch controls fast synaptic vesicle exocytosis.

Jiong Tang1, Anton Maximov, Ok-Ho Shin

  • 1The Center for Basic Neuroscience, UT Southwestern Medical Center, Dallas, TX 75390, USA.

Cell
|September 23, 2006
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Summary

Calcium (Ca2+) binding to synaptotagmin 1 triggers fast neurotransmitter release by displacing complexins from SNARE complexes. This mechanism explains the speed and synchronicity of Ca2+-triggered exocytosis.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Fast Ca(2+)-triggered exocytosis of synaptic vesicles is crucial for neurotransmission.
  • Synaptotagmin 1 and complexins are key proteins involved in this process, both binding to SNARE complexes.
  • The precise functional coupling between synaptotagmin 1 and complexins remains unclear.

Purpose of the Study:

  • To elucidate the molecular mechanism coupling synaptotagmin 1 and complexin functions in fast Ca(2+)-triggered exocytosis.
  • To investigate the role of complexin binding in activating SNARE complexes.
  • To determine how Ca(2+) binding to synaptotagmin 1 initiates vesicle release.

Main Methods:

  • Biochemical assays to study protein-protein interactions between synaptotagmin 1, complexins, and SNARE complexes.
  • In vitro experiments demonstrating Ca(2+)-dependent displacement of complexin by synaptotagmin 1.
  • Physiological experiments manipulating complexin concentration to assess its impact on exocytosis.

Main Results:

  • Synaptotagmin 1 competes with complexin for binding to SNARE complexes.
  • Ca(2+) binding to synaptotagmin 1 causes the displacement of complexin from SNARE complexes.
  • Increased complexin levels selectively inhibit fast Ca(2+)-triggered exocytosis while preserving other SNARE-dependent fusion events.

Conclusions:

  • Complexin binding activates SNARE complexes into a metastable state.
  • Ca(2+)-induced displacement of complexin by synaptotagmin 1 triggers fast exocytosis.
  • This mechanism explains complexin's role in fast neurotransmitter release and its high speed and synchronicity.