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Many changes produced by chronic stress are similar to those seen in cannabinoid CB1 receptor–deficient mice. In the current study, we examined both anxiety-like behavior and dendritic complexity within the prefrontal cortex and basolateral amygdala (BLA) in wild-type and CB1 receptor–deficient mice, under basal conditions and following exposure to 21 days of protracted restraint stress. CB1 receptor–deficient mice exhibited increased indices of anxiety in the elevated plus maze under basal conditions that were similar in magnitude to changes seen in wild-type mice exposed to chronic stress. Chronic stress or deletion of the CB1 receptor also produced a reduction in both apical dendritic length and branch points of neurons within layer II/III of the prelimbic region of the prefrontal cortex. Pyramidal neurons in the (BLA) of CB1 receptor–deficient mice were found to have increased dendritic length compared with wild type. Chronic stress increased dendritic length of these amygdalar neurons in both wild-type and CB1 receptor–deficient mice. Collectively, these data demonstrate that loss of cannabinoid CB1 receptor signaling produces a chronic stress-like phenotype under basal conditions and provide a putative neural substrate that may subserve the changes in emotional behavior seen following disruption of CB1 receptor signaling.