Abstract
Interactions between the basal ganglia and the cerebral cortex are critical for normal goal-directed behavior. In the present study, we used immediate-early genes (c-fos, zif 268) as functional markers to investigated how basal ganglia output altered by stimulation/blockade of D1 dopamine receptors in the striatum affects cortical function. Systemic administration of the mixed D1/D2 receptor agonist apomorphine (3 mg/kg) increased immediate-early gene expression in the striatum and throughout most of the cortex. Unilateral intrastriatal infusion of the selective D1 receptor antagonist SCH-23390 (0.5-10 microg) blocked this response bilaterally in striatum and cortex in a dose-dependent manner. Even apparently regionally restricted blockade of striatal D1 receptors attenuated gene expression throughout striatum and cortex in both hemispheres. Intrastriatal administration of the D1 antagonist inhibited apomorphine-induced sniffing/whisking, whereas other motor behaviors were unaffected. To determine whether such changes in cortical gene expression could reflect altered cortical function, we examined the effects of blocking striatal D1 receptors on whisker stimulation-evoked immediate-early gene expression in the sensorimotor cortex. Apomorphine increased sensory stimulation-evoked gene expression in the barrel cortex, and intrastriatal infusion of SCH-23390 attenuated this effect. These results suggest that stimulation of D1 dopamine receptors in the striatum exerts a widespread facilitatory effect on cortical function.