Consistent with previous findings (Takahashi and Castillo, 2006; Hoffman et al., 2006), in non-stress animals, WIN application reliably decreased excitatory neurotransmission in a CB1-dependent manner. The observed WIN-induced increase in fEPSPs in CMS animals is surprising given that CMS reliably downregulates hippocampal CB1 in adult animals (Hill et al., 2005; Hill et al., 2008b; Reich et al, 2009). We originally hypothesized that WIN should produce less inhibition on glutamate neurotransmission in stress animals because of a decrease in CB1 levels. However, this hypothesis assumes that CMS equally affects all CB1, regardless of residence. Being that CB1 density is ten-fold higher at CCK-GABAergic terminals than at glutamatergic terminals, this scenario also proposes that CB1 modulation of both terminal types is scaled as an attempt to maintain a homeostatic balance. Thus, an average CMS-induced reduction in the general hippocampal CB1 population, as demonstrated through either western blot or binding analysis (Hill et al., 2005; Hill et al., 2008b; Reich et al, 2009), may not be representative of individual populations (i.e. GABAergic or glutamatergic). Indeed, pharmacological isolation of CB1 function on glutamatergic terminals,
