INVESTIGADORES
TARAVINI Irene Rita Eloisa
congresos y reuniones científicas
Título:
Immunodetection of pleiotrophin in striatal interneurons and nigral dopaminergic neurons
Autor/es:
TARAVINI IR; FERRARIO JE; DELBE J; COURTY J; MURER MG; GERSHANIK OS; RAISMAN-VOZARI R
Lugar:
Innsbruck, Austria
Reunión:
Congreso; 20th Biennal Meeting of the International Society for Neurochemistry and the European Society for Neurochemistry; 2005
Institución organizadora:
International Society for Neurochemistry and the European Society for Neurochemistry
Resumen:
Parkinson’s disease is characterized by a selective damage of the dopaminergic nigrostriatal pathway. Surviving neurons undergo both spontaneous and levodopa induced plastic changes. We have recently reported an increased expression of Pleiotrophin (PTN) in the striatum of rats with a unilateral 6-OHDA lesion of the nigrostriatal tract chronically treated with levodopa. Interestingly, recent reports have shown that PTN stimulates the differentiation of dopaminergic mesencephalic neurons in vitro. The aim of this study was to identify the cellular types that contain PTN in the striatum and substantia nigra (SN) and to detect the presence of the PTN receptor N-syndecan in the SN. Using double-immunofluorescence we found PTN to colocalize with NeuN but not with GFAP in the striatum. Immunolabeling of PTN with specific markers for interneuronal subpopulations at this level ruled out calretinin (+) and parvalbumin (+) GABAergic neurons. Conversily around 40% of PTN immunolabeled neurons corresponded to GABAergic interneurons that contain nitric oxide synthase (NOS) and somatostatin (SST), while around 60% of them were cholinergic interneurons. We also studied the distribution of the N-syndecan in the SN and found it to colocalize with TH. Our results indicate that PTN is selectively localized in cholinergic interneurons and GABAergic interneurons that express SST/NOS in the striatum. At the SN both PTN and N-syndecan are present in a small number of dopaminergic neurons. In conjunction, these results suggest that PTN would possibly mediate some of the compensatory mechanisms that surviving dopaminergic nigrostriatal neurons undergo in the parkinsonian brain.