brain AEA levels with FAAH inhibitors failed to alter either cue- or stress-induced relapse to ethanol-seeking behavior. These results are not surprising given the number of studies reporting increased AEA levels that persist following chronic ethanol. Together the data from reinstatement experiments support the involvement of CB1 in cue-induced relapse behavior, but more work needs to be conducted to determine the neuroanatomical loci of the effects of SR to reduce reinstatement. In addition, future studies will need to consider the role of ECs in mediating relapse to ethanol self-administration.
