Reinstatement studies provide clear evidence that CB1 activation is involved in cue-induced but not stress-induced relapse. However, no studies to date have employed strategies to understand which neuroanatomical structures are responsible for the effects of SR to block reinstatement of ethanol-seeking. Considering the role the EC system plays in regulating VTA burst firing, it is possible that CB1 activation may contribute to the DA release observed in response to drug-paired cues (Schultz, 1998). However, the complete lack of any data regarding the function of the EC system in discrete brain regions during cued-reinstatement renders this hypothesis as utter speculation. As a consequence, much work needs to be done to elucidate the mechanisms by which this important neuromodulatory system contributes to relapse.
