62 and PND 70; a period when CB1 levels are stabilizing to adult levels (Lee and Gorzalka, 2012). We chose this age range to approximate mid-adolescence to young adulthood in humans (Spear 2000; Lee and Gorzalka, 2012). Notably, starting with animals ranging from PND 42 to PND 49, Hu et al., (2011) observed a reduction in DSI, following a 21 day CRS protocol. In comparison, changes in hippocampal CB1 were not observed in rats, PND 35–45, subjected to 10 days of CRS; although receptor downregulation was observed in adult animals, PND 75–85 (Lee and Hill, 2012). The latter result is consistent with previous findings with the CMS protocol in adult animals (Hill et al., 2005; Hill et al., 2008b; Reich et al, 2009), suggesting a developmental regulation of stress-endocannabinoid interactions. Interestingly, Lee and Hill (2012) did observe an approximate 30–40% increase in Kd values in both adolescent and adult animals following CRS. Even though they report this change as non-significant, it contrasts with early observations that changes in Kd were not concomitant with decreases in hippocampal CB1 following exposure to CMS (Hill et al., 2008b; Hill et al., 2005). Furthermore, CB1 upregulation was observed following a 40 day recovery period
