Traumatic brain injuries (TBI) are a major cause of disability amongst military service members. In addition to combat-related head injuries, military personnel are vulnerable to repetitive blast-related TBIs due to the frequent use of small explosive charges for breaching and training. However, little is known about the functional consequences or recovery after repeated blast exposure. Here, we tested the hypothesis that repeated exposure to low intensity blasts results in deficits of sensorimotor gating and memory. Male Sprague-Dawley rats were exposed to repeated blasts using a compressed gas shockwave tube. Sensorimotor gating was assessed with prepulse inhibition (PPI) across tactile, visual, and auditory modalities. PPI was tested at baseline and 1, 3, and 7 days after blast exposure to assess acute effects and recovery. To identify dose response effects, both the number of blasts (5, 10, or 15 repetitions) and the blast intensity (7.5, 15, or 25 pounds per square inch, PSI) were varied. Blast effects on memory were assessed via contextual and cued fear conditioning, and acquisition and retention of fear extinction 2-weeks post-blast. Repetitive exposure to 15-25 PSI blasts transiently disrupted PPI across multiple sensory modalities, with minimal effects on baseline startle and no effects of 7.5-PSI. The 25-PSI blast also disrupted contextual fear memory "dose" dependently with repeated blasts. These data suggest PSI levels well within scaling parameters of low-level blast exposure in humans (e.g. flashbang) can induce acute sensorimotor gating and contextual memory deficits. Future research is needed to understand the mechanisms and trajectory of these effects.