Thus, a pronounced species difference appears to be present between the effects of stress on endocannabinoid signaling in mice and rats. In rats, stress appears to mobilize 2-AG signaling, while suppressing AEA signaling, in a variety of limbic structures. In mice, there does not appear to be an effect of stress on 2-AG (at least through the examination of tissue levels of endocannabinoid content), while the reduction in AEA still seems to be present. The effects of acute stress on central endocannabinoid content can be seen in Table 1. Interestingly, while no studies have been performed on central endocannabinoid content following stress exposure in humans, we have recently reported that exposure of women to the Trier social stress test results in a rapid increase in circulating levels of 2-AG while not affecting circulating levels of AEA (Hill et al., 2009d), suggesting that stress-induced mobilization of 2-AG is a conserved mechanism from rats to humans
