A single in-vivo exposure to delta 9THC blocks endocannabinoid-mediated synaptic plasticity.
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 Delta 9-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.
Mato
Susana
S
Equipe INSERM Avenir, Plasticité synaptique: Maturation & Addiction, Institut Magendie des Neurosciences, Rue Camille Saint Saëns, 33077 Bordeaux, France.
Chevaleyre
Vivien
V
Robbe
David
D
Pazos
Angel
A
Castillo
Pablo E
PE
Manzoni
Olivier J
OJ
D000818:Animals; D063385:Cannabinoid Receptor Modulators / Q000037:antagonists & inhibitors* / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D013759:Dronabinol / Q000008:administration & dosage*; D063388:Endocannabinoids; D006624:Hippocampus / Q000187:drug effects / Q000502:physiology; D066298:In Vitro Techniques; D051379:Mice; D009473:Neuronal Plasticity / Q000187:drug effects* / Q000502:physiology; D009714:Nucleus Accumbens / Q000187:drug effects / Q000502:physiology; D013569:Synapses / Q000187:drug effects* / Q000502:physiology
D063385:Cannabinoid Receptor Modulators; D063388:Endocannabinoids; D013759:Dronabinol