IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v410y2001i6828d10.1038_35069076.html
   My bibliography  Save this article

Endogenous cannabinoids mediate retrograde signalling at hippocampal synapses

Author

Listed:
  • Rachel I. Wilson

    (University of California)

  • Roger A. Nicoll

    (University of California)

Abstract

Marijuana affects brain function primarily by activating the G-protein-coupled cannabinoid receptor-1 (CB1)1,2,3, which is expressed throughout the brain at high levels4. Two endogenous lipids, anandamide and 2-arachidonylglycerol (2-AG), have been identified as CB1 ligands5,6. Depolarized hippocampal neurons rapidly release both anandamide and 2-AG in a Ca2+-dependent manner6,7,8. In the hippocampus, CB1 is expressed mainly by GABA (γ-aminobutyric acid)-mediated inhibitory interneurons, where CB1 clusters on the axon terminal9,10,11. A synthetic CB1 agonist depresses GABA release from hippocampal slices10,12. These findings indicate that the function of endogenous cannabinoids released by depolarized hippocampal neurons might be to downregulate GABA release. Here we show that the transient suppression of GABA-mediated transmission that follows depolarization of hippocampal pyramidal neurons13 is mediated by retrograde signalling through release of endogenous cannabinoids. Signalling by the endocannabinoid system thus represents a mechanism by which neurons can communicate backwards across synapses to modulate their inputs.

Suggested Citation

  • Rachel I. Wilson & Roger A. Nicoll, 2001. "Endogenous cannabinoids mediate retrograde signalling at hippocampal synapses," Nature, Nature, vol. 410(6828), pages 588-592, March.
    • Handle: RePEc:nat:nature:v:410:y:2001:i:6828:d:10.1038_35069076
    DOI: 10.1038/35069076
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/35069076
    File Function: Abstract
    Download Restriction: Access to the full text of the articles in this series is restricted.
    File URL: https://libkey.io/10.1038/35069076?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.

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Thomas Heinbockel & Ze-Jun Wang, 2015. "Cellular Mechanisms of Action of Drug Abuse on Olfactory Neurons," IJERPH, MDPI, vol. 13(1), pages 1-11, December.
    2. John D. Harvey & Thomas Heinbockel, 2018. "Neuromodulation of Synaptic Transmission in the Main Olfactory Bulb," IJERPH, MDPI, vol. 15(10), pages 1-11, October.

    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:410:y:2001:i:6828:d:10.1038_35069076. 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.