acute stressor (restraint) augmented depolarization-induced-suppression of inhibition (DSI), a short-term endocannabinoid-mediated plasticity of GABAergic neurotransmission in the rat hippocampus. This enhancement in endocannabinoid (eCB) signaling was due to a glucocorticoid (GC)-induced increase in 2-AG levels. Similar increases in eCB signaling and eCB-mediated plasticity are found in the mouse amygdala following 10 days of chronic restraint stress (Patel at al., 2009; Sumislawski et al., 2011). Despite these reports on stress-induced facilitation of eCB signaling, the predominant observation is that stress attenuates eCB signaling and eCB-mediated synaptic plasticity in the striatum, hypothalamus, nucleus accumbens and hippocampus (Rossi et al., 2008; Wamsteeker et al., 2010; Wang et al., 2010; Hu et al., 2011). For example, 21 days of chronic restraint stress impairs DSI in the rodent hippocampus (Hu et al., 2011). Thus, it appears that while stress generally affects the eCB system, the type and duration of stressor may determine the direction of the stress effect on a given brain structure; an important consideration when comparing across studies.
