In rats, acute systemic administration of CB1 agonists, (e.g. WIN 55,212-2 and HU210) prior to extinction learning have been shown to facilitate fear extinction (Lin et al., 2008; Lin et al., 2006; Lin et al., 2009; Pamplona et al., 2008; Pamplona et al., 2006); but see (Chhatwal et al., 2005)) and prevent spontaneous recovery of extinguished conditioned fear responses (Lin et al., 2006). In addition, cannabidiol, a non-psychoactive phytocannabinoid, and pharmacological agents that enhance levels of released eCBs, such as AM404, an eCB reuptake inhibitor, and URB597, a fatty acid amide hydrolase (FAAH) inhibitor that blocks hydrolysis of anandamide, have been shown to facilitate within-session extinction learning (Bitencourt et al., 2008; Varvel et al., 2007), enhance the retention of extinction (Bitencourt et al., 2008; Chhatwal et al., 2005; de Oliveira Alvares et al., 2008; Lin et al., 2009; Varvel et al., 2007) and also decrease the recovery of conditioned fear responses in rats (Chhatwal et al., 2005) if given prior to extinction learning. Conversely, co-administration of CB1 antagonists, such as AM251 and rimonabant [SR141716], block the extinction enhancing effects of
