An important caveat in interpreting the current findings is the age of the animals. Rat adolescence, liberally defined as ~PND 28 to ~ PND 55 (Spear, 2000), is marked by a maturational process of neuronal reorganization and refinement. The endocannabinoid system also undergoes significant maturation during this period. Despite reported variations, brain CB1 and endocannabinoid function generally increase during early development, peaking with the onset of adolescence, then decreasing through adolescence and finally stabilizing in early adulthood- PND 70 (Lee and Gorzalka, 2012). In the present study, it is possible that our observations occurred during this late adolescent decline in CB1 levels. In this scenario, an increase in CB1 density, binding affinity or efficacy in response to CMS exposure may explain the proposed gain in GABAergic CB1 function. However, at the time of electrophysiological experiments, our animals are between PND 62 and PND 70; a period when CB1 levels are stabilizing to adult levels (Lee and Gorzalka, 2012). We chose this age range to approximate mid-adolescence to young adulthood in humans (Spear 2000; Lee and Gorzalka, 2012). Notably, starting with
