glycogen and Huntington-Disease

Injection of excitotoxins, such as quinolinic acid (QA), into the striatum has been extensively used as an experimental model of Huntington's disease, while injection of 6-hydroxydopamine (6-OHDA) into the dopaminergic nigrostriatal pathway provides a well established model of Parkinson's disease. In the present study, we have examined the metabolic changes induced by an intrastriatal injection of QA or 6-OHDA using histochemical staining for the metabolic markers cytochrome oxidase (COx) and active glycogene phosphorylase (GPa). Intrastriatal injection of QA produced major changes in COx (decrease of staining) and GPa (increase of staining, except in the core of the lesion where the staining was virtually absent) histochemistry at the level of the striatum and of most of the other basal ganglia nuclei. Although attenuated over time, these changes persisted up to one year after the lesion. On the contrary, after the intrastriatal injection of 6-OHDA (which induces only a partial lesion of the nigrostriatal pathway), we did not observe any remarkable changes in COx or GPa staining. This study illustrates the discrepancies between the morphological changes and metabolic changes that are induced when using these experimental models of neurodegenerative disorders.

Topics: Animals; Autoradiography; Benzazepines; Biomarkers; Corpus Striatum; Disease Models, Animal; Dopamine Antagonists; Dopamine Uptake Inhibitors; Electron Transport Complex IV; Glycogen; Huntington Disease; Male; Mazindol; Microinjections; Nerve Degeneration; Oxidopamine; Parkinson Disease; Phosphorylase a; Quinolinic Acid; Radioligand Assay; Rats; Rats, Sprague-Dawley; Receptors, Dopamine; Sympatholytics; Tritium