A Pilot Study On Behavioral Testing And Event-related Potential P300in Rats With Traumatic Brain Injury

【Background】How to identify the traumatic brain injury induced cognitivedysfunction is still one of difficult puzzles in forensic clinical identification. Itsmechanism has not been understood so far. Mental scale methods of assessment couldnot identify aggravation, disguise, and so on. Therefore, the keys to explain itsmechanism might lie in the selection of appropriate animal model, and determinationof objective measurements.【Objects】The first aim of this study was to make the experimental model of ratswith traumatic brain injury induced cognitive dysfunction. Then escape latency inMorris water maze, latency and amplitude of P300were recorded and analyzed todetermine the objective indicators of cognitive dysfunction.【Methods】Male SD rats were selected and randomly divided into five groups.Control group received no treatment. Sham-operated group was surgically preparedbut received no trauma. Operation groups received adaptive feeding, respectively, for3d,7d and14d after a nonpenetrating impact to the left cranium. Spatial learningabilities were assessed for4d using Morris water maze spatial navigation tasks andescape latency was recorded. Spatial memory abilities were assessed using Morriswater maze spatial exploration tasks and the frequency of crossing platform wasrecorded. Rats after anesthesia completed an passive auditory novelty oddballparadigm while latency and amplitude of P300were recorded. All data were analyzedwith software SPSS11.5. 【Results】Typical P300potential could be observed in each groups. P300latencymeans of control, sham-operated, postoperative day3and7and14groups were305.29±34.03ms,324.33±31.30ms,446.67±49.09ms,474.00±42.05ms and388.33±22.37ms, respectively. There was no significant difference between controland sham-operated groups (P=0.38). Operation groups showed longer P300latencythan control and sham-operated groups (P＜0.01). Although the P300latencies ofpostoperative day3and7groups were not different (P=0.28), they were longer thanthose of postoperative day14group (P≤0.04). P300amplitude means of control,sham-operated, postoperative day3and7and14groups were26.97±5.83μV,25.18±6.79μV,17.03±5.54μV,15.35±6.89μV and14.77±3.51μV, respectively.There was no significant difference between control and sham-operated groups(P=0.60). The P300amplitude decreased significantly after treatment (P＜0.05).However, operation groups did not differ in P300amplitude. Escape latency in eachgroup declined while spatial navigation training increased. There was no significancebetween control and sham-operated groups (P=0.19). Operation groups showedlonger escape latency than control and sham-operated groups (P＜0.01). There wereno significantly difference between postoperative day3and7groups (P=0.826).Postoperative day14group displayed longer escape latency than postoperative day3and7groups (P＜0.05). The frequency of crossing platform was no significantlydifference between control and sham-operated groups. The frequency of crossingplatform significantly decreased in operation groups. There was significantly positivecorrelation between Morris water maze escape latency and P300latency (r=0.606,P=0.002). However, Morris water maze escape latency was not significantlycorrelated with P300amplitude.【Conclusions】Morris water maze escape latency could reflect the cognitivedysfunction of SD rats with traumatic brain injury. Auditory event-related potentialP300was closely related with cognitive dysfunction induced by traumatic brain injury. The experimental model of SD rats in this study might play an important role infollow-up studies.