Binge eating disorder (BED) is characterized by uncontrollable episodes of eating in a short period of time, with a subjective loss of control of overconsumption behavior. The role CB2 cannabinoid receptor (CB2R) plays in binge-like intake has not yet been identified. In this regard, the present study aims to evaluate the effect of the administration of CB2R agonist, antagonist, or both on binge-like intake of palatable food (PF) in adolescent mice. We used 35 C57BL6/J male mice of 30 postnatal days in this research
all animals were housed individually and had ad libitum access to a standard diet (SD) and water. Animals were evaluated for a total of 15 sessions of the Binge Eating Test (BET), which consisted of 1 h access to PF (chocolate sandwich cookies) according to intermittent diet protocol, with one-day access/one-day no-access. PF and SD caloric intake, as well as the PF binge index (defined as consuming ≥20% of total caloric intake per day during the 1 h access to PF), were analyzed. Mice were randomly assigned to one of the following treatment groups: (1) control
(2) vehicle
(3) HU308, selective CB2R agonist
(4) AM630, selective CB2R antagonist
(5) AM630+HU308 coadministration of antagonist and agonists of CB2R. All treatments were administered intraperitoneally before BET sessions. Our results show that HU308 significantly reduced binge-like intake of PF, while no significant differences were found in the rest of the groups. These results suggest that activation of the CB2R decreases the binge-like intake in adolescent mice and that chronic overconsumption in conditions of non-homeostatic feeding can be modulated by the CB2R. Furthermore, the activation of CB2R may also modulate reward pathways, reducing binge-like behavior, which could be further explored in future studies as a treatment for BED.