Brief Communication | Published:

A single in-vivo exposure to Δ9THC blocks endocannabinoid-mediated synaptic plasticity

Nature Neuroscience volume 7, pages 585586 (2004) | Download Citation

Subjects

Abstract

Endogenous cannabinoids (eCB) mediate synaptic plasticity in brain regions involved in learning and reward. Here we show that in mice, a single in-vivo exposure to Δ9-tetrahydrocannabinol (THC) abolishes the retrograde signaling that underlies eCB-mediated synaptic plasticity in both nucleus accumbens (NAc) and hippocampus in vitro. This effect is reversible within 3 days and is associated with a transient modification in the functional properties of cannabinoid receptors.

Access optionsAccess options

Rent or Buy article

Get time limited or full article access on ReadCube.

from$8.99

All prices are NET prices.

References

  1. 1.

    , , & Nature 411, 583–587 (2001).

  2. 2.

    , , & Neuron 37, 577–582 (2003).

  3. 3.

    , , & J. Neurosci. 22, 2074–2082 (2002).

  4. 4.

    & Neuron 38, 461–472 (2003).

  5. 5.

    , , , & Proc. Natl. Acad. Sci. USA 99, 8384–8388 (2002).

  6. 6.

    & Br. J. Pharmacol. 140, 781–789 (2003).

  7. 7.

    Pharmacol. Ther. 95, 153–164 (2002).

  8. 8.

    et al. Br. J. Pharmacol. 125, 1567–1577 (1998).

  9. 9.

    & Nature 410, 588–592 (2001).

  10. 10.

    , & Neuron 29, 729–738 (2001).

  11. 11.

    , & Eur. J. Neurosci. 17, 1747–1754 (2003).

  12. 12.

    et al. Brain Res. Mol. Brain Res. 46, 100–108 (1997).

  13. 13.

    et al. J. Neurochem. 73, 2447–2459 (1999).

  14. 14.

    , , & J. Neurosci. 16, 8057–8066 (1996).

  15. 15.

    , , & J. Neurosci. 23, 4815–4820 (2003).

Download references

Acknowledgements

Work in O.J.M.'s laboratory is supported by grants from INSERM, Ministère de la Recherche, Fondation pour le Recherche Médicale and Région Aquitaine. P.E.C.'s laboratory is supported by grants from NIH (National Institute on Drug Abuse) and the Pew Charitable Trust.

Author information

Author notes

    • David Robbe

    Present address: Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, New Jersey 07102, USA.

    • Susana Mato
    •  & Vivien Chevaleyre

    These authors contributed equally to this work.

Affiliations

  1. Equipe INSERM Avenir, Plasticité synaptique: Maturation & Addiction, Institut Magendie des Neurosciences, Rue Camille Saint Saëns, 33077 Bordeaux, France.

    • Susana Mato
    • , David Robbe
    •  & Olivier J Manzoni
  2. Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461, USA.

    • Vivien Chevaleyre
    •  & Pablo E Castillo
  3. Department of Physiology and Pharmacology, University of Cantabria, Santander 39011, Cantabria, Spain.

    • Angel Pazos

Authors

  1. Search for Susana Mato in:

  2. Search for Vivien Chevaleyre in:

  3. Search for David Robbe in:

  4. Search for Angel Pazos in:

  5. Search for Pablo E Castillo in:

  6. Search for Olivier J Manzoni in:

Competing interests

The authors declare no competing financial interests.

Corresponding authors

Correspondence to Pablo E Castillo or Olivier J Manzoni.

Supplementary information

PDF files

  1. 1.

    Supplementary Fig. 1

    In both the Nac and the CA1 region of the hippocampus, a single THC injection (3 mg/kg) is not sufficient to uncouple CB1R from Gi/o proteins. CB1R-stimulation of [35S]GTPγS binding with the CB-agonist WIN55,212-2 (100μM) in the NAc and hippocampus CA1 demonstrates unaltered cannabinoid agonist-stimulated activation of Gi/o proteins after single THC exposure (vehicle white bars; THC black bars). Coincubation in the presence of SR141716-A (10μM) prevented the stimulatory effect of WIN55,212-2 (100μM) in sections from both groups indicating the involvement of CB1Rs (not shown).

  2. 2.

    Supplementary Methods

About this article

Publication history

Received

Accepted

Published

DOI

https://doi.org/10.1038/nn1251

Further reading