Acute organophosphate (OP) intoxication evokes status epilepticus and is associated with the development of chronic impairments such as spontaneous recurrent seizures (SRS). A growing body of evidence suggests that neuroinflammation may contribute to the development of chronic sequelae following acute OP intoxication. The mTOR signaling pathway is highly implicated in both immune and epileptogenic processes. Thus, we evaluated the activation of mTOR in a rat model of acute OP intoxication and probed the involvement of mTOR signaling in OP-induced neuroinflammation and epileptogenesis. Adult male Sprague-Dawley rats were acutely intoxicated with OP diisopropylfluorophosphate (DFP) and treated with standard medical countermeasures. mTOR activity is transiently enhanced in the hippocampus within 1 hour post exposure, returning to baseline at 3 days post exposure. Elevated mTOR activity is observed in microglial populations, suggesting the involvement of mTOR in DFP-induced neuroinflammation. Inhibition of mTOR attenuated DFP-induced microglial activation, further implicating mTOR activity in neuroinflammatory processes following acute OP intoxication. Moreover, preliminary data suggest that mTOR inhibition may suppress the development of SRS following DFP intoxication.