Unaltered lactate and glucose transporter levels in the MPTP mouse model of Parkinson's disease.

摘要: Background: Metabolic impairment contributes to development of Parkinson’s disease (PD). Mitochondrial dysfunction is involved in degeneration nigral dopamine neurons. Also, PD there are alterations glucose metabolism nigro-striatal pathways, and increased cerebral lactate levels have been found. Objectives: We raise the question whether changes amount transporters energy substrates pathogenesis PD. Methods: used confocal immunofluorescence immunogold postembedding electron microscopic techniques study altered for monocarboxylates (MCT1 MCT2) (GLUT1) MPTP mouse model Results: found that MCT1 GLUT1 were densely located blood vessel endothelium, while MCT2 was present perivascular astrocytic end feet processes substantia nigra striatum control mice. localisation densities MCTs unaltered model. Discussion: This first reporting on distribution metabolic Our results suggest that, although impairments PD, MCT1, not changed following dopaminergic neurodegeneration. contrast findings other neurodegenerative disease, such as mesial temporal lobe epilepsy, where large MCT levels.