To investigate the role of dopamine release in cognitive impairment and motor learning deficits after brain injury, different levels of traumatic brain injury (TBI) were made in rats by using fluid percussion at two different atmospheres (2 Psi and 6 Psi). Tonic and phasic bursting dopamine release and behavior tests followed at several time points. We used in vitro fast-scan cyclic voltammetry to survey dopamine release in the striatum and analyzed the rats’ behavior using novel object recognition (NOR) and rotarod tests. Both tonic and bursting dopamine release were greatly depressed in the severely (6 Psi) injured group, which persisted up to 8 weeks later. However, in the 2 Psi-injured group, the suppression of bursting dopamine release occurred at 1~2 weeks after injury, but there were no significant differences after 4 weeks. Tonic dopamine release was also diminished significantly at 1~2 weeks after the injury; partial recovery could then be seen 4 weeks after injury. A significant deficiency in the fixed speed rotarod test and NOR test were noted in both 2 Psi and 6 Psi groups initially; however, the changes recovered in the 2 Psi group 2 weeks after injury while persisting in the 6 Psi group. In conclusion, striatal evoked dopamine release was affected by fluid percussion injury, with behavioral deficits showing differences as a function of injury severity. The severe fluid percussion injury (6 Psi) group showed more dopamine release defects, as well as cognitive and motor deficiencies. Recovery of dopamine release and improvement in behavioral impairment were better in the mild TBI group.
