IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v401y1999i6755d10.1038_44586.html
   My bibliography  Save this article

P/Q-type calcium channels mediate the activity-dependent feedback of syntaxin-1A

Author

Listed:
  • Kathy G. Sutton

    (Biotechnology Laboratory and Dept Psychiatry University of British Columbia)

  • John E. McRory

    (Biotechnology Laboratory and Dept Psychiatry University of British Columbia)

  • Heather Guthrie

    (Biotechnology Laboratory and Dept Psychiatry University of British Columbia)

  • Timothy H. Murphy

    (Kinsmen Laboratory of Neurological Research, Dept Psychiatry University of British Columbia)

  • Terrance P. Snutch

    (Biotechnology Laboratory and Dept Psychiatry University of British Columbia)

Abstract

Spatial and temporal changes in intracellular calcium concentrations are critical for controlling gene expression in neurons1,2,3,4,5. In many neurons, activity-dependent calcium influx through L-type channels stimulates transcription that depends on the transcription factor CREB by activating a calmodulin-dependent pathway6,7,8,9,10,11. Here we show that selective influx of calcium through P/Q-type channels12,13,14 is responsible for activating expression of syntaxin-1A, a presynaptic protein that mediates vesicle docking, fusion and neurotransmitter release. The initial P/Q-type calcium signal is amplified by release of calcium from intracellular stores and acts through phosphorylation that is dependent on the calmodulin-dependent kinase CaM K II/IV, protein kinase A and mitogen-activated protein kinase kinase. Initiation of syntaxin-1A expression is rapid and short-lived, with syntaxin-1A ultimately interacting with the P/Q-type calcium channel to decrease channel availability. Our results define an activity-dependent feedback pathway that may regulate synaptic efficacy and function in the nervous system.

Suggested Citation

  • Kathy G. Sutton & John E. McRory & Heather Guthrie & Timothy H. Murphy & Terrance P. Snutch, 1999. "P/Q-type calcium channels mediate the activity-dependent feedback of syntaxin-1A," Nature, Nature, vol. 401(6755), pages 800-804, October.
    • Handle: RePEc:nat:nature:v:401:y:1999:i:6755:d:10.1038_44586
    DOI: 10.1038/44586
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/44586
    File Function: Abstract
    Download Restriction: Access to the full text of the articles in this series is restricted.
    File URL: https://libkey.io/10.1038/44586?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    As the access to this document is restricted, you may want to search for a different version of it.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:nature:v:401:y:1999:i:6755:d:10.1038_44586. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.