In a recent study from our lab, CMS exposure during adolescence selectively enhanced hippocampal-dependent fear conditioning in male rats. This enhancement in aversive learning was prevented by exogenous CB1 activation (Reich et al., 2013). These findings are consistent with previous observations that peri-adolescent/adolescent exposure to chronic stress alters CB1 signalling in the hypothalamus, amygdala and prefrontal cortex (Wamsteeker et al., 2010; Lee and Hill 2012). To date, these are the only three studies that directly address the effects of adolescent stress on the eCB system. This is surprising, given that adolescence is a period of neuronal maturation that is highly vulnerable to stress (Spear, 2000; Lee and Gorzalka, 2012). Exploring the relationship between stress and eCB signalling during this developmental period may assist in elucidating the etiology of stress-related pathologies such as Major Depressive Disorder and PTSD. Using hippocampal fEPSP recordings from adolescent male animals exposed to CMS, we hypothesized that CMS-downregulation of CB1 would impair function on both glutamatergic and GABAergic synapses. However, we observed that CMS does not affect glutamate-CB1 function directly but does increase glutamatergic neurotransmission through
