19 ± 0.49 rotations per min, dopamine-grafted + nimodipine = 1.67 ± 0.54 rotations per min, sham-grafted = 3.92 ± 1.08 rotations per

min; late post-graft: dopamine-grafted = 1.69 ± 0.51 rotations per min, dopamine-grafted + nimodipine = 1.58 ± 0.57 rotations per min, sham-grafted = 5.67 ± 0.78 rotations per min; F2,33 = 22.716, P = 0.001; Fig. 3A). Analysis of levodopa-induced rotational behavior between dopamine-grafted rats receiving nimodipine or vehicle pellets revealed no significant difference (P = 0.941) PLX4032 nmr in this behavior that is easily reversed by dopamine cell replacement. Analysis of levodopa-induced rotational behavior in sham-grafted rats receiving nimodipine or vehicle pellets revealed no significant difference between groups (early post-graft: sham-grafted = 3.08 ± 1.17 rotations per min, sham-grafted + nimodipine = 0.75 ± 0.45

rotations Akt inhibitor review per min; mid post-graft: sham-grafted = 3.92 ± 1.08 rotations per min, sham-grafted + nimodipine = 2.33 ± 0.69 rotations per min; late post-graft: sham-grafted = 5.67 ± 0.78 rotations per min, sham-grafted + nimodipine = 4.36 ± 0.88 rotations per min; F1,22 =2.101, P = 0.161; Fig. 3B). Analysis of behavior on the vibrissae-evoked forelimb placement task found a significant difference between sham-grafted, dopamine-grafted, and dopamine-grafted rats receiving nimodipine pellets (F2,75 = 3.937, P = 0.024). While all groups showed 95% or greater impairment at an early post-graft time-point, dopamine-grafted rats receiving nimodipine pellets showed significantly greater improvement than grafted rats receiving vehicle pellets (P = 0.001) and sham-grafted rats (P = 0.001) at the latest time-point post-grafting

(successful taps per 10 trials: sham-grafted = 0 ± 0, dopamine-grafted = 0.06 ± 0.06, dopamine-grafted + nimodipine = 3.75 ± 1.37; Fig. 4A). Analysis of behavior on the vibrissae-evoked forelimb placement Olopatadine task found no significant difference between rats receiving nimodipine or vehicle pellets (F1,18 = 0.411, P = 0.529) in the absence of a dopamine graft. Both groups showed no impairment prior to 6-OHDA delivery (successful taps per 10 trials: sham-grafted = 10 ± 0, sham-grafted + nimodipine = 10 ± 0), but significant stable and equal degree of impairment at early (successful taps per 10 trials: sham-grafted = 0 ± 0, sham-grafted + nimodipine = 0 ± 0) and late time-points post-lesion (successful taps per 10 trials: sham-grafted = 0 ± 0, sham-grafted + nimodipine = 0.08 ± 0.08; Fig. 4B). Analysis of levodopa-induced dyskinesias found that while there was a small and gradual sensitization of dyskinesia in sham-grafted rats there was a significant blunting of dyskinesia in both dopamine-grafted groups (Fig. 5A). There was a significant difference between groups (F2,33 = 33.012, P = 0.001), with both dopamine-grafted groups differing significantly from sham-grafted rats at all time-points examined (P = 0.001).