Abstract
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.