Interestingly, subsequent studies employing rats instead of mice (which is the species employed by Tasker and colleagues for their in vitro work), found quite different results. An initial study from the group of Andrea Hohmann found that brief exposure to a foot shock stress resulted in a dramatic and rapid elevation in both AEA and 2-AG levels within the periaqueductal grey (Hohmann et al., 2005). Additional studies using the model of acute restraint stress in rats produced results more consistent with those seen by Tasker and colleagues, than what was seen in the studies employing mice. Specifically, 30 minute exposure to restraint stress in rats was found to produce an elevation in 2-AG levels in the PFC, hippocampus and hypothalamus (Hill et al., 2007), but not within the amygdala (Hill et al., 2009c). Interestingly, AEA content was correspondingly found to be reduced by stress within the PFC (Hill et al., 2007) hippocampus (Hill et al., 2007) and the amygdala (Hill et al., 2009c), but not the hypothalamus (Hill et al., 2007). This reduction in AEA, at least within the amygdala,
