Affiliations: Glio- and Neurotransmitter Group, Centre for Molecular Biology and Neuroscience and Institute for Basic Medical Sciences, University of Oslo, Oslo, Norway | Department of Pathology, Oslo University Hospital-Ullevål. Oslo, Norway | The Brain and Muscle Energy Group, Centre for Molecular Biology and Neuroscience and Institute for Basic Medical Sciences, University of Oslo, Oslo, Norway | Department of Neuroscience and Pharmacology, University of Copenhagen, Copenhagen, Denmark | Center for Healthy Aging, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark | Department of Neurology, Oslo University Hospital, Norway | Department of Oral Biology, University of Oslo, Norway
Abstract: Background: Metabolic impairment contributes to development of Parkinson's disease (PD). Mitochondrial dysfunction is involved in degeneration of nigral dopamine neurons. Also, in PD there are alterations in glucose metabolism in nigro-striatal pathways, and increased cerebral lactate levels have been found. Objectives: We raise the question of whether changes in the amount transporters of energy substrates are involved in the pathogenesis of PD. Methods: We have used confocal immunofluorescence and immunogold postembedding electron microscopic techniques to study whether there are altered levels of the transporters for monocarboxylates (MCT1 and MCT2) and glucose (GLUT1) in the MPTP mouse model of PD. Results: We found that MCT1 and GLUT1 were densely located in blood vessel endothelium, while MCT2 was present in perivascular astrocytic end feet processes in the substantia nigra and the striatum of control mice. We found that the localisation and densities of MCTs and GLUT1 were unaltered in the PD model. Discussion: This is the first study reporting on the distribution of metabolic transporters in PD. Our results suggest that, although there are metabolic impairments in PD, the levels of MCT1, MCT2 and GLUT1 is not changed following dopaminergic neurodegeneration. This is in contrast to findings in other neurodegenerative disease, such as mesial temporal lobe epilepsy, where there are large alterations in MCT levels.