Amantadine improves water maze performance without affecting motor behavior following traumatic brain injury in rats.

摘要: Amantadine, a dopamine agonist, is reported to have beneficial effects on the neurobehavioral sequelae of clinical brain injury. However, there are currently no published laboratory reports its use in assessment functional or histopathological outcome following experimental traumatic injury (TBI). To this end, we examined daily amantadine treatment recovery (motor and Morris water maze performance) hippocampal neuronal survival controlled cortical impact (CCI) (4 meters/sec, 2.7 mm tissue deformation). Male Sprague-Dawley rats were pretrained motor performance tasks (beam balance beam walking) one day prior tested post-operative days 1-5. Additionally, all subjects trained 14-18. Beginning after CCI sham surgery, animals injected once for 18 with either (10 mg/kg, i.p.) saline. The regimen was ineffective promoting increasing neurons both CA1 CA3 regions TBI, but did show improved swim latencies during five testing (Day 14 vs. Day 18, p < 0.01) when compared saline controls. Mean (+/- SE) 15.12 +/- 2.8, 13.25 4.18, 70.83 11.1, 38.5 3.55 sec sham/saline, sham/amantadine, injured/saline, injured/amantadine groups, respectively. Thus, while administration exhibited neutral effect behavior, it produced modest attenuation deficits. This latter finding consistent data suggesting therapy.