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, via inhibiting GABAergic neurotransmission, results in a similar WIN-induced fEPSP reduction observed in non-stress animals. This suggests that glutamatergic-CB1 function is spared by CMS and is consistent with other reports demonstrating that different stressors modulate CB1 physiology on GABAergic terminals but not glutamatergic in the amygdala and striatum (Rossi et al., 2008; Patel at al., 2009; Sumislawski et al., 2011). However, chronic stress did impair eCB-mediated glutamatergic neurotransmission in both the hypothalamus (Wamsteeker et al., 2010) and in the nucleus accumbens (Wang et al., 2010). Blocking CB1 with AM251 prevents the WIN effects on fEPSP magnitude in all conditions; demonstrating that these effects are CB1 dependent. This argues against the possibility that WIN is acting either on CB2 receptors or other non-CB1 sites in stress animals.
