This chapter summarizes the results of studies conducted by our laboratory on the long-term impact of Δ9-tetrahydrocannabinol (Δ9-THC), the intoxicating constituent of cannabis, on adolescent mice and rats. The primary objective of these studies was to explore potential causal links between teenage cannabis use and subsequent changes in adult cognition, psychosocial functioning, and metabolism, which have been consistently documented by epidemiological research. We begin by discussing the need for ecologically valid animal models of adolescent Δ9-THC exposure, which take into consideration factors such as exposure intensity and inherent differences across species, sexes, and the animal lifespan. We then detail findings from a model designed to replicate, in male and female mice and rats, daily but moderately intense cannabis use in human adolescents. Placed within the context of existing literature, the results obtained with this model indicate that adolescent exposure to Δ9-THC causes enduring changes in endocannabinoid signaling associated with profound deficits in microglial activity, synaptic plasticity, and memory, as well as dysfunctions in energy metabolism. The findings highlight adolescence as a critical period of vulnerability to Δ9-THC and point to several possible avenues for future human research.