Corticofugal fibres from the prefrontal, prelimibic and anterior sensorimotor cortices were transected by a wide coronal knife-cut through the forceps minor. The cut was performed on the dopamine-depleted side of unilaterally 6-hydroxydopamine-lesioned rats, or on either the right or the left side of intact rats. Sham-lesioned controls received a superficial cortical cut at the same level. Seven days after surgery, apomorphine (0.25 mg/kg s.c.) was administered to 6-hydroxydopamine-lesioned animals and D-amphetamine (5 mg/kg i.p.) was administered to the non-dopamine-denervated ones. Two hours later, the animals were perfusion-fixed for the immunohistochemical detection of the nuclear protein Fos. A computerized image analysis technique was used to quantify, bilaterally, striatal Fos expression in 11 areas of the striatum. The frontocortical transection reduced both apomorphine- and amphetamine-induced Fos expression by 33-66% within the ipsilateral caudate-putamen. The effect was observed throughout the rostral portion of the striatal complex, where the lesioned cortical fibres terminate most densely. A separate batch of unilaterally 6-hydroxydopamine-lesioned rats was used to test the effect of frontocortical transection on amphetamine-and apomorphine-induced turning behaviour. Two groups of rats, showing similar rates of contralateral turning (7-8 turns/min) in response to apomorphine (0.25 mg/kg s.c.), were subjected to either a complete frontocortical transection or a sham lesion on the dopamine-denervated side. An additional two groups, showing comparable rates of ipsilateral turning (15 turns/min) in response to amphetamine (5 mg/kg i.p.), received similar lesions, but now on the side ipsilateral to the intact dopaminergic innervation. The frontocortical transection reduced both apomorphine- and amphetamine-induced turning by, on average, 40%, while the sham lesion had no effect. The present findings suggest that the full expression of dopamine-receptor-induced Fos activation and turning behaviour depends on an intact glutamatergic corticostriatal input.