Levodopa treatment induces changes in the expression of Pleiotrophin receptors in a rat model of Parkinson’s disease.

FERRARIO JE; SALDAÑA ORTEGA M; TARAVINI IR; MURER MG; HUNOT S; GERSHANIK O; RAISMAN-VOZARI R

Kyoto, Japón

Congreso; 10th International Congress of Parkinson`s Disease and Movement Disorders; 2006

The Movement Disorder Society

Parkinson’s disease (PD) is characterized by selective damage to the dopaminergic nigrostriatal pathway. Surviving neurons undergo both spontaneous and levodopa induced plastic changes. We have recently identified Pleiotrophin (PTN) mRNA as being increased in the lesioned striatum of hemiparkinsonian rats after a long term treatment with levodopa (Ferrario et al. 2004). In addition, it has been shown that PTN enhances the maturation of dopaminergic neurons in vitro (Mourlevat et al. 2005). This data, among others, suggest that PTN may be a new modulatory factor for dopaminergic neurons, and consequently, may contribute to the plastic adaptations of dopaminergic neurotransmission in the damaged striatum. Thus, the PTN receptors involved in this function might represent a crucial pharmacological target in the treatment of PD. Two well known receptors of PTN in the brain are:  the heparan sulfate proteoglycan N-syndecan (N-syn) and the receptor protein tyrosine phosphatase z/β (RPTP z/β). To go beyond our previous observations in vitro, we analyzed the changes in expression of PTN and its receptors in the dopaminergic system, by quantitative real time reverse transcription PCR on total RNA purified from striatal and ventral mesencephalon of rats lesioned with intrastriatal 6-OHDA, which were treated either with vehicle or levodopa for 21 days. In addition, we completed these studies with a histological characterization of PTN and N-Syndecan at the mesencephalon of normal rats.