The serotonin (5-HT) system is emerging as a key player in the appearance of L-DOPA-induced dyskinesia (LID). We have shown that removal of the 5-HT neurons by toxin lesion, or silencing of their activity by 5-HT1A/1B receptor agonists suppress already established dyskinesia in the rat and monkey models of Parkinson´s disease (PD). Transplantation of embryonic dopamine cells has been tested in clinical trials in PD patients. Appearance of the so-called graft-induced dyskinesia (GID) in a subset of grafted patients has contributed to prevent further investigation of this approach. In light of the role of the 5-HT system in the appearance of LID and of the recent finding showing the presence of an intense 5-HT hyperinnervation in grafted patients, it has been raised the possibility that the 5-HT system may play a role also in this form of dyskinesia. Inclusion of 5-HT cells among in the graft may thus affect success of the transplantation approach to PD. Indeed, the partial 5-HT1A agonist buspirone has been shown to suppress GID in a small group of grafted patients. We have now investigated the involvement of the 5-HT system in the appearance of GID in the rat model, where dyskinesias are induced in grafted emi-parkinsonian animals upon administration of low amphetamine doses. Data show that the 5-HT system is involved in this form of dyskinesias, but also that mechanisms underlying their appearance extend beyond this system. Detailed results will be presented at the meeting.