Blast injuries, that is
injuries caused by the complex pressure wave generated by some explosions, show increasing frequency throughout the world. However, whether
blast injury is capable of inducing memory dysfunction has not been previously investigated. The present study examines the effects of
blast injury-induced neurotrauma on
memory deficit in rats. Furthermore, it is hypothesized that
blast injury, stimulating
nitric oxide production in the medial mesodiencephalic reticular formation and the dorsal hippocampus, both structures being involved in memory processing, may induce
memory deficits. Prior to
blast injury, Wistar rats were trained for an active avoidance task for 6 days. On day 6, rats that had acquired the avoidance response were subjected to whole-body
blast injury, using a BT-I
shock tube. Neurotrauma was confirmed by electron microscopical examination. At the completion of cognitive testing, rats were sacrificed at 3, 24 hours and 5 days after injury. The
nitric oxide production in the brain structures was determined by the total
nitrite/
nitrate concentration, and by the expression of
inducible nitric oxide synthase mRNA. The rats with
blast injury revealed significant deficits in performance of the active avoidance task that persisted up to 5 days post-injury. Electron microscopical findings in both brain structures showed swellings of neurons, glial reaction, myelin debris, and increased pinocytotic activity on the fifth day following
trauma. In blast injured rats, there was a significant elevation in total
nitrite/
nitrate levels 3 and 24 hours following injury which was comparable with the changes in the expression of
inducible nitric oxide synthase mRNA. The results indicate that
blast injury-induced neurotrauma is able to cause cognitive deficits.