Mild traumatic brain injury (TBI) is a common public health burden affecting otherwise young and healthy individuals. In spite of this, TBI is underreported due to the transient nature of clinical symptoms. Although the overt symptoms like unconsciousness dissipate quickly, less obvious symptoms at the cellular level (including inflammation and excitotoxicity) persist weeks post-TBI. These cellular changes are associated with behavioral alterations including anxiety, depression, and excessive alcohol consumption. There are currently no therapeutic interventions for mild TBI, however, the endocannabinoid system is a promising therapeutic target due to its well-known anti-inflammatory role. Previously we showed that inhibition of monoacylglycerol lipase (MAGL), the enzyme involved in 2-acylglycerol (2-AG) degradation, with JZL184 following mild TBI attenuated neuroinflammation and synaptic hyperexcitability up to two weeks post-TBI. The aim of this study was to examine if common behavioral pathologies resulting from mTBI, including anxiety, pain sensitivity, cognitive deficits, and alcohol drinking, could be reversed during the acute recovery period up to two weeks post-TBI. Adult male Wistar rats underwent a 5-mm left lateral craniotomy, and TBI was induced three days later by lateral fluid percussion. Thirty minutes post-TBI, rats received intraperitoneal injections of vehicle (alcohol, emulphor, and saline; 1:1:18) or JZL184 (16 mg/kg). Resulting experimental groups were sham surgery (n=10), TBI-VEH (n=10), and TBI-JZL (n=10). Anxiety-like behavior (open field test), cognitive deficits (Y-maze), pain sensitivity (Von Frey test), and motivated alcohol drinking (progressive ratio operant self-administration) were assessed up to two weeks post-TBI. JZL184 administered-TBI animals had significantly improved cognitive performance (p<0.001 compared to cognitively impaired rats; one sample T-test) and reduction in mechanical sensitivity to pain (p=0.2; two-way ANOVA) compared to vehicle-injected TBI animals. JZL184 administration led to a significant reduction in anxiety-like behavior (p<0.05; one way ANOVA) and a reduction in motivated alcohol drinking (p= 0.2; one-way ANOVA) compared to TBI-Vehicle animals. Together with our previous data, these results show that EC degradation inhibition 30 minutes post-TBI has potential therapeutic benefits that persist throughout the acute recovery period up to 14 days post-injury. Current studies are investigating the mechanisms of EC degradation inhibition-mediated improvements from TBI.