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 in CRS-exposed animals, despite no apparent change immediately following the stress (Lee and Hill, 2012). The Kd and recovery data suggest that stress-induced plasticity in CB1 function may not be observed as changes in receptor density. Thus, in the present study, enhanced CB1 function (or decreased function – Hu et al., 2011) would not necessarily be inconsistent with a lack of change in overall receptor density (see above discussion on efficacy). However, as previously noted, the type and duration of stress protocols as well as animal age may produce incongruent results and should be considered when cross-interpreting. For example, a 10 day CRS exposure in juvenile rats (PND 21–30), resulted in a desensitization of CB1 on GABAergic terminals in the hypothalamus, but not in the hippocampus (Wamsteeker et al., 2010). These findings agree with Lee and Hill (2012), but are inconsistent with the current study. Wamsteeker et al. used a 5 sec depolarization step (−70 mv to +20 mv) to
