A role for eCB signaling in alcohol-induced suppression of BA stimulated activation of nucleus accumbens neurons has also been demonstrated (Perra et al., 2005). Alcohol was shown to depressed BA-evoked spike probability in nucleus accumbens neurons, an effect reversed by SR141716 which, when administered alone had no effect on BA-evoked spike probability in nucleus accumbens neurons. The FAAH inhibitor URB597 also inhibited the alcohol-induced suppression of BLA-evoked spike probability in nucleus accumbens neurons. Interestingly, treatment with the CB1 receptor agonist Win 55212-2 15–20 hours before alcohol treatment reduced the alcohol-induced suppression of BLA-stimulated spike probability in nucleus accumbens neurons. This effect was not due to a functional tolerance as the dose-response curves for Win 55212-2-induced suppression of BLA-evoked spike probability in nucleus accumbens neurons was not different between control rats and rats treated with Win 55212-2 15–20 hours earlier (Perra et al., 2005). These data suggest a role for eCB signaling in alcohol-induced suppression of BLA-evoked spike probability in nucleus accumbens neurons and further suggest that CB1 receptor activity can modulate BA efferent neurotransmission.
