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The Journal of Neuroscience, December 14, 2005, 25(50):11619-11627; doi:10.1523/JNEUROSCI.2294-05.2005

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Cellular/Molecular
Presynaptic Homeostatic Plasticity Rescues Long-Term Depression after Chronic {Delta}9-Tetrahydrocannabinol Exposure

Susana Mato,1 David Robbe,1 Nagore Puente,2 Pedro Grandes,2 and Olivier J. Manzoni1

1Institut National de la Santé et de la Recherche Médicale Equipe Avenir (Plasticité Synaptique: Maturation and Addiction), Institut Magendie des Neurosciences, 33077 Bordeaux Cedex, France, and 2Department of Neurosciences, Faculty of Medicine and Dentistry, Basque Country University, 699-48080 Bilbao, Spain

Alterations of long-term synaptic plasticity have been proposed to participate in the development of addiction. To preserve synaptic functions, homeostatic processes must be engaged after exposure to abused drugs. At the mouse cortico-accumbens synapses, a single in vivo injection of {Delta}9-tetrahydrocannabinol (THC) suppresses endocannabinoid-mediated long-term depression. Using biochemical and electrophysiological approaches, we now report that 1 week of repeated in vivo THC treatment reduces the coupling efficiency of cannabinoid CB1 receptors (CB1Rs) to Gi/o transduction proteins, as well as CB1R-mediated inhibition of excitatory synaptic transmission at the excitatory synapses between the prefrontal cortex and the nucleus accumbens (NAc). Nonetheless, we found that cortico-accumbens synapses unexpectedly express normal long-term depression because of a reversible switch in its underlying mechanisms. The present data show that, in THC-treated mice, long-term depression is expressed because a presynaptic mGluR2/3 (metabotropic glutamate receptor 2/3)-dependent mechanism replaces the impaired endocannabinoid system. Thus, in the NAc, a novel form of presynaptic homeostasis rescues synaptic plasticity from THC-induced deficits.

Key words: accumbens; cannabinoids; metabotropic glutamate receptor; glutamate; mice; LTD; long-term depression

Received June 6, 2005; revised September 27, 2005; accepted October 18, 2005.






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