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Regional characterization of energy metabolism in the brain of normal and MPTP-intoxicated mice using new markers of glucose and phosphate transport.
Lagrue E., Abe H., Lavanya M., Touhami J., Bodard S., Chalon S., Battini J.-L., Sitbon M., Castelnau P.
Journal of Biomedical Science 17, 1 (2010) 91 - http://www.hal.inserm.fr/inserm-00617219
 (21129221) 
Regional characterization of energy metabolism in the brain of normal and MPTP-intoxicated mice using new markers of glucose and phosphate transport.
Emmanuelle Lagrue1, 2, Hiroyuki Abe3, 4, Madakasira Lavanya3, 5, Jawida Touhami3, Sylvie Bodard1, Sylvie Chalon1, Jean-Luc Battini3, Marc Sitbon () 3, Pierre Castelnau () 1, 2
1:  Imagerie et cerveau
INSERM : U930 – Université François Rabelais - Tours – CNRS : ERL3106
Hôpital Bretonneau 1 Bd Tonnelle 37044 Tours
France
2:  Unité de neuropédiatrie
Centre de compétence Maladies mitochondriales – Hôpital Clocheville - Pôle Enfants – CHRU Tours
F-37044 Tours, France
France
3:  IGMM - Institut de génétique moléculaire de Montpellier
http://www.igm.cnrs-mop.fr/
CNRS : UMR5535 – Université Montpellier II - Sciences et techniques
1919 Route de Mende 34293 MONTPELLIER CEDEX 5
France
4:  Department of anatomy
Teikyo University – School of Medicine
2-11-1 Kaga, Itabashi-ku, Tokyo 173-8605
Japan
5:  Department of microbiology
University of Pennsylvania
Philadelphia, PA 19104-6142, USA
United States
The gibbon ape leukemia virus (GALV), the amphotropic murine leukemia virus (AMLV) and the human T-cell leukemia virus (HTLV) are retroviruses that specifically bind nutrient transporters with their envelope glycoproteins (Env) when entering host cells. Here, we used tagged ligands derived from GALV, AMLV, and HTLV Env to monitor the distribution of their cognate receptors, the inorganic phosphate transporters PiT1 and PiT2, and the glucose transporter GLUT1, respectively, in basal conditions and after acute energy deficiency. For this purpose, we monitored changes in the distribution of PiT1, PiT2 and GLUT1 in the cerebellum, the frontal cortex, the corpus callosum, the striatum and the substantia nigra (SN) of C57/BL6 mice after administration of 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridinium (MPTP), a mitochondrial complex I inhibitor which induces neuronal degeneration in the striato-nigral network.The PiT1 ligand stained oligodendrocytes in the corpus callosum and showed a reticular pattern in the SN. The PiT2 ligand stained particularly the cerebellar Purkinje cells, while GLUT1 labelling was mainly observed throughout the cortex, basal ganglia and cerebellar gray matter. Interestingly, unlike GLUT1 and PiT2 distributions which did not appear to be modified by MPTP intoxication, PiT1 immunostaining seemed to be more extended in the SN. The plausible reasons for this change following acute energy stress are discussed.These new ligands therefore constitute new metabolic markers which should help to unravel cellular adaptations to a wide variety of normal and pathologic conditions and to determine the role of specific nutrient transporters in tissue homeostasis.
Life Sciences
Life Sciences/Food and Nutrition
English
1021-7770

Article in peer-reviewed journal
10.1186/1423-0127-17-91
Journal of Biomedical Science (J Biomed Sci)
Publisher BioMed Central
ISSN 1021-7770 (eISSN : 1423-0127)
international
2010
2010-12-04
17
1
91

1-Methyl-4-phenyl-1 – 2 – 3 – 6-tetrahydropyridine – Animals – Biological Markers – Biological Transport – Brain – Gene Products – env – Glucose Transporter Type 1 – Human T-lymphotropic virus 1 – Leukemia Virus – Gibbon Ape – Murine – Ligands – Mice – Inbred C57BL – Receptors – Virus – Sodium-Phosphate Cotransporter Proteins – Type III
HA was supported by a post-doctoral fellowship from ARC (Association pour la Recherche contre le Cancer) and ML by successive fellowships from AFM (Association Française pour les Myopathies) and ARC (Association pour la Recherche sur le Cancer). MS was supported by a Contrat d'Interface INSERM-CHU. Part of this work has been funded by ARC (Association pour la Recherche sur le Cancer) and Fondation de France.
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