Dopamine D1 receptor activation maintains motor coordination in injured rats but does not accelerate the recovery of the motor coordination deficit

The sensorimotor cortex and the striatum are interconnected by the corticostriatal pathway, suggesting that cortical injury alters the striatal function that is associated with skilled movements and motor learning, which are functions that may be modulated by dopamine (DA). In this study, we explored motor coordination and balance in order to investigate whether the activation of D1 receptors (D1Rs) modulates functional recovery after cortical injury. The results of the beam-walking test showed motor deficit in the injured group at 24, 48 and 96 h post-injury, and the recovery time was observed at 192 h after cortical injury. In the sham and injured rats, systemic administration of the D1R antagonist SCH-23390 (1 mg/kg) alone at 24, 48, 96 and 192 h significantly (P < 0.01) increased the motor deficit, while administration of the D1R agonist SKF-38393 alone (2, 3 and 4 mg/kg) at 24, 48, 96 and 192 h post-injury did not produce a significant difference; however, the co-administration of SKF-38393 and SCH-23390 prevented the antagonist-induced increase in the motor deficit. The cortical + striatal injury showed significantly increased the motor deficit at 24, 48, 96 and 192 h post-injury (P < 0.01) but did not show recovery at 192 h. In conclusion, the administration of the D1R agonist did not accelerate the motor recovery, but the activation of D1Rs maintained motor coordination, confirming that an intact striatum may be necessary for achieving recovery.