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Related Experiment Videos

Synaptotagmin IX regulates Ca2+-dependent secretion in PC12 cells.

Mitsunori Fukuda1, Judith A Kowalchyk, Xiaodong Zhang

  • 1Laboratory for Developmental Neurobiology, Brain Science Institute, RIKEN (The Institute of Physical and Chemical Research), 2-1 Hirosawa, Wako, Saitama 351-0198, Japan. mnfukuda@brain.riken.go.jp

The Journal of Biological Chemistry
|December 26, 2001
PubMed
Summary

Synaptotagmin IX (Syt IX) compensates for Synaptotagmin I (Syt I) deficiency in PC12 cells, regulating calcium-dependent norepinephrine release. Both Syt IX and Syt I are crucial for dense-core vesicle exocytosis.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Synaptotagmin I (Syt I) is a key calcium sensor for neurotransmitter release.
  • Syt I-deficient PC12 cells exhibit normal calcium-dependent norepinephrine (NE) release, suggesting alternative calcium sensors exist.

Purpose of the Study:

  • To identify alternative calcium sensors involved in NE release in Syt I-deficient PC12 cells.
  • To investigate the role of Synaptotagmin IX (Syt IX) in dense-core vesicle exocytosis.

Main Methods:

  • Screening Syt I-deficient PC12 cells for other Syt isoforms.
  • Utilizing antibodies against Syt IX and Syt I C2A domains in permeable PC12 cells.

Main Results:

  • Synaptotagmin IX (Syt IX) was identified as an abundant dense-core vesicle protein in Syt I-deficient PC12 cells.

Related Experiment Videos

  • Syt IX is essential for calcium-dependent NE release from PC12 cells.
  • Antibodies against Syt IX or Syt I inhibited NE release, confirming their roles in exocytosis.

    • Conclusions:

    • Synaptotagmin IX (Syt IX) functions as a calcium sensor for norepinephrine release in PC12 cells.
    • Syt proteins may act cooperatively and redundantly in dense-core vesicle exocytosis.