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

TY - JOUR

T1 - Unaltered lactate and glucose transporter levels in the MPTP mouse model of Parkinson's disease

AU - Puchades, Maja

AU - Sogn, Carl Johan

AU - Maehlen, Jan

AU - Bergersen, Linda H

AU - Gundersen, Vidar

PY - 2013/1/1

Y1 - 2013/1/1

N2 - 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.

AB - 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.

KW - Animals

KW - Astrocytes

KW - Brain Chemistry

KW - Fluorescent Antibody Technique

KW - Glucose Transport Proteins, Facilitative

KW - Glucose Transporter Type 1

KW - Humans

KW - Immunohistochemistry

KW - MPTP Poisoning

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Microscopy, Confocal

KW - Microscopy, Electron

KW - Monocarboxylic Acid Transporters

KW - Neostriatum

KW - Parkinson Disease

KW - Substantia Nigra

KW - Symporters

KW - Tyrosine 3-Monooxygenase

U2 - 10.3233/jpd-130190

DO - 10.3233/jpd-130190

M3 - Journal article

C2 - 23963315

SN - 1877-7171

VL - 3

SP - 371

EP - 385

JO - Journal of Parkinson's Disease

JF - Journal of Parkinson's Disease

IS - 3

ER -