Autism spectrum disorder is characterized by a wide range of symptoms, including impairments in social interactions, communication, and emotion-related behavior. In this study we aimed to uncover the changes of inhibitory basket cell outputs in the prefrontal cortex and basolateral amygdala, regions that play a central role in the expression of core symptoms in autistic behaviors.We observed that valproate treatment at E12.5 resulted in a decrease in ultrasound vocalizations in the pups (n=12) and an increase in tactile sensitivity assessed by the von Frey test in comparison to controls (n=13). As young adults, valproate treated mice showed decreased sociability and social novelty seeking in the three chamber test. After the behavior tests, the density of type 1 cannabinoid receptor (CB1) and parvalbumin (PV) containing inhibitory axon terminals was analyzed. We found that in valproate treated mice, the density of CB1+, but not PV+, axon terminals was significantly increased in the lateral and basal amygdala. Furthermore, in layer 1 of the prelimbic cortex, the density of CB1+, but not of PV+ axon terminals was significantly increased. These data imply that the endocannabinoid signaling system controlling GABAergic synaptic communication is altered in mice treated with valproate during development.