are short-lived. Indeed, 2-AG levels peak at 20 minutes following the start of the 10th restraint exposure and, by 60 minutes, are almost back to control levels (Patel et al., 2009). Similar effects were observed in rats, where 24 hours after the 10th restraint exposure, 2-AG levels are not different from control (Hill et al., 2010b). These data suggest that levels of 2-AG surge in response to stress, and that if the stress is repeated in a predictable fashion, each surge gets progressively larger. However, between surges, 2-AG levels return to baseline. In addition to restraint stress, administration of chronic corticosterone to rats increases levels of 2-AG in the amygdala (Hill et al., 2005), nonetheless, acute corticosterone treatment produced only a non-significant trend toward 2-AG elevation (Hill et al., 2010a).
