ArticleJournal of biomedical science2010
Regional characterization of energy metabolism in the brain of normal and MPTP-intoxicated mice using new markers of glucose and phosphate transport.
Article in Journal of biomedical science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Neuronal alkaline phosphatase promotes the spread of Tau-induced pathology, and its blockade prevents neurodegeneration and memory loss.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Brain Calcifications: Genetic, Molecular, and Clinical Aspects.International journal of molecular sciences · 2023Review
- Identification of Copper Transporter 1 as a Receptor for Feline Endogenous Retrovirus ERV-DC14.Journal of virology · 2022Article
- Shared cerebral metabolic pathology in non-transgenic animal models of Alzheimer's and Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- PiT2 regulates neuronal outgrowth through interaction with microtubule-associated protein 1B.Scientific reports · 2017Article
- Neuroprotective effect of 5-aminolevulinic acid against low inorganic phosphate in neuroblastoma SH-SY5Y cells.Scientific reports · 2017Article
- Cardiac cell proliferation assessed by EdU, a novel analysis of cardiac regeneration.Cytotechnology · 2016Article
- Mutations in XPR1 cause primary familial brain calcification associated with altered phosphate export.Nature genetics · 2015Article
- Loss of function of Slc20a2 associated with familial idiopathic Basal Ganglia calcification in humans causes brain calcifications in mice.Journal of molecular neuroscience : MN · 2013Article
- Analysis of gene expression pattern and neuroanatomical correlates for SLC20A2 (PiT-2) shows a molecular network with potential impact in idiopathic basal ganglia calcification ("Fahr's disease").Journal of molecular neuroscience : MN · 2013Article
- Association between a novel mutation in SLC20A2 and familial idiopathic basal ganglia calcification.PloS one · 2013Article
- Genome-wide association mapping of loci for antipsychotic-induced extrapyramidal symptoms in mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2012Article
- Mutations in SLC20A2 link familial idiopathic basal ganglia calcification with phosphate homeostasis.Nature genetics · 2012Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.