GABAergic imbalance is normalized by dopamine D 1 receptor activation in the striatum contralateral to the cortical injury in motor deficit-recovered rats.

Rationale: The sensorimotor cortex and the striatum are interconnected by the corticostriatal pathway, suggesting that cortical injury alters the striatal function, which may be modulated by dopamine.
Objectives: We studied whether the activation of dopamine D ₁ receptors (D ₁ Rs) modulates the γ-aminobutyric acid (GABA) and glutamate levels in the striatum of recovered rats at 192 h after cortical injury.
Methods: The D ₁ R agonist SKF-38393 (0, 2, 3, or 4 mg/kg) was administered at 24, 48, 96, and 192 h post-injury, and then rats were decapitated to determine GABA and glutamate levels and the levels of D ₁ R mRNA on both sides of the striatum.
Results: GABAergic imbalance in the striatum contralateral to the injury site was normalized by the administration of the D ₁ R agonist, but this treatment did not produce a significant effect on glutamate levels, suggesting that glutamate was metabolized into GABA. The administration of SKF-38393 (2 mg/kg) decreased the levels of D ₁ R mRNA in the striatum contralateral to the injury, and this effect was blocked by the coadministration of the D ₁ R antagonist SCH-23390 (2 mg/kg). In the striatum ipsilateral to the injury, the D ₁ R agonist increased the D ₁ R mRNA levels, an effect that was blocked by SCH-23390.
Conclusion: The reversal of the GABAergic imbalance in the striatum contralateral to the cortical injury can be modulated by extrastriatal D ₁ R activation, and the D ₁ R agonist-induced increases in the D ₁ R mRNA levels in the striatum ipsilateral to the injury suggest that the striatum may be necessary to achieve functional recovery.