In this paradigm, post-conditioning CS+ presentation caused a stimulus-locked discharge in BLA-responsive mPFC neurons, which was absent upon CS− presentation. Systemic CB1 receptor activation by WIN 55,212-2 (0.5m/kg; i.v.), before conditioning, dramatically potentiated neuronal associative learning to the CS+ as demonstrated by both increased neuronal burst frequency and spikes within each burst event compared to saline treatment (Laviolette and Grace, 2006b). This effect was blocked by systemic co-administration of the CB1 receptor antagonist, AM251 (1.0mg/kg; i.v.). Given that cortical neuronal bursting has been hypothesized to represent the processing of reward-related learning cues, memory encoding, as well as decision-making, these results suggest that CB1 receptor signaling modulates the active encoding and expression of associative learning in BLA-responsive mPFC neurons (Laviolette and Grace, 2006b).
