Striatal and Cortical Neurochemical Changes Induced by Chronic Metabolic Compromise in the 3-Nitropropionic Model of Huntington's Disease
- 1 August 2002
- journal article
- Published by Elsevier in Neurobiology of Disease
- Vol. 10 (3) , 410-426
- https://doi.org/10.1006/nbdi.2002.0512
Abstract
No abstract availableKeywords
This publication has 75 references indexed in Scilit:
- Novel therapies in the search for a cure for Huntington's diseaseProceedings of the National Academy of Sciences, 2001
- Deficits in Striatal Dopamine D2 Receptors and Energy Metabolism Detected by in Vivo MicroPET Imaging in a Rat Model of Huntington's DiseaseExperimental Neurology, 2000
- Energetics in the pathogenesis of neurodegenerative diseasesPublished by Elsevier ,2000
- Severe deficiencies in dopamine signaling in presymptomatic Huntington's disease miceProceedings of the National Academy of Sciences, 2000
- Dopamine D1 and D2 receptor gene expression in the striatum in Huntington's diseaseAnnals of Neurology, 1997
- Striatal glucose metabolism and dopamine D2 receptor binding in asymptomatic gene carriers and patients with Huntington's diseaseBrain, 1996
- Effects of BDNF and NT‐4/5 on Striatonigral Neuropeptides or Nigral GABA Neurons In VivoEuropean Journal of Neuroscience, 1996
- Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acidJournal of Neuroscience, 1993
- Decrease in mRNA levels but not in the density of D2 dopamine receptors in rat striatum after transient forebrain ischemiaNeuroscience Letters, 1991
- Transient forebrain ischemia produces multiple deficits in dopamine D1 transmission in the lateral neostriatum of the ratBrain Research, 1989