the endocannabinoid/endovanniloid, Anandamide (AEA), in the hippocampus, amygdala, striatum, medial prefrontal cortex and hypothalamus (Gorzalka and Hill, 2011). Conversely, the other major endocannabinoid (eCB), 2-arachidonoyl-glycerol (2-AG), is transiently enhanced by chronic or acute restraint stress but is either reduced or not affected by chronic mild stress (Gorzalka and Hill, 2011; Wang et al., 2012). This differential modulation of eCBs is intriguing considering that 2-AG mediates depolarization-induced-suppression-of-inhibition (DSI), a short-term suppression of GABA release caused by eCB signaling (Kano et al., 2009), whereas AEA is involved in the tonic activation of CB1 (Kim and Alger, 2010). Indeed, chronic stress is capable of impairing both short and long-term eCB synaptic plasticities in the striatum, hypothalamus, nucleus accumbens and hippocampus (Rossi et al., 2008; Wamsteeker et al., 2010; Wang et al., 2010; Hu et al., 2011), although 10 days of chronic restraint stress enhances eCB signaling in the amygdala (Patel et al., 2009; Sumislawski et al., 2011). Notably, these stress effects on eCB function are mimicked by administration of chronic corticosterone to animals (Hill et al., 2008a; Bowles et al., 2011) and blocked by antagonizing glucocorticoid receptors (Gorzalka and Hill, 2011). Thus, stress appears to modulate eCB signaling via the Hypothalamic-Pituitary-Adrenal-Axis (HPA), which
