Journal
JOURNAL OF NEUROSCIENCE
Volume 30, Issue 21, Pages 7236-7248Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0736-10.2010
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Funding
- National Institutes of Health/National Institute on Drug Abuse
- National Alliance for Research on Schizophrenia and Depression
- Basque Country Government [GIC07/70-IT-432-07]
- Red de Trastornos Adictivos, Redes Temeticas de Investigacion Cooperativa en Salud, Instituto de Salud Carlos III, Ministerio de Ciencia e Innovacion [RD07/0001/2001]
- Basque Country University
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Similar to dopamine (DA), cannabinoids strongly influence prefrontal cortical functions, such as working memory, emotional learning, and sensory perception. Although endogenous cannabinoid receptors (CB(1)Rs) are abundantly expressed in the prefrontal cortex (PFC), very little is known about endocannabinoid (eCB) signaling in this brain region. Recent behavioral and electrophysiological evidence has suggested a functional interplay between the dopamine and cannabinoid receptor systems, although the cellular mechanisms underlying this interaction remain to be elucidated. We examined this issue by combining neuroanatomical and electrophysiological techniques in PFC of rats and mice (both genders). Using immunoelectron microscopy, we show that CB(1)Rs and dopamine type 2 receptors (D(2)Rs) colocalize at terminals of symmetrical, presumably GABAergic, synapses in the PFC. Indeed, activation of either receptor can suppress GABA release onto layer 5 pyramidal cells. Furthermore, coactivation of both receptors via repetitive afferent stimulation triggers eCB-mediated long-term depression of inhibitory transmission (I-LTD). This I-LTD is heterosynaptic in nature, requiring glutamate release to activate group I metabotropic glutamate receptors. D(2)Rs most likely facilitate eCB signaling at the presynaptic site as disrupting postsynaptic D2R signaling does not diminish I-LTD. Facilitation of eCB-LTD may be one mechanism by which DA modulates neuronal activity in the PFC and regulates PFC-mediated behavior in vivo.
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