Effect of dopaminergic denervation and transplant-derived reinnervation on a marker of striatal GABAergic function

Solid grafts of dopamine-containing fetal mesencephalon were placed adjacent to the striatum of rats with 6-hydroxydopamine lesions of ascending dopaminergic projections. These grafts resulted in a significant, although partial, reversal of the lesion-induced increase in striatal glutamic acid decarboxylase (GAD) when measured 3-4 months after the lesion. These results suggest that the grafted neurons can partly restore inhibitory control over striatal GABA neurons. In the same rats, the grafts partially reversed apomorphine-induced turning although amphetamine-induced turning was nearly abolished. It is likely that both apomorphine-induced behavior and striatal GAD activity reflect the sustained chronic influence of the graft on target neurons in striatum.