title: Sensory-motor performance after acute glutathione depletion by L-buthionine sulfoximine injection into substantia nigra pars compacta.
abstract: Glutathione is the major antioxidant in the living cells. Its deficit has been linked to neurodegenerative disorders as Parkinson's disease but its role in the etiology of nigral degeneration and sensory-motor performance has been poorly explored. To evaluate the effect of glutathione depletion on nigro-striatal oxidative metabolism and sensory-motor performance in rats, l-buthionine sulfoximine (15 mM) or saline solution was injected into substantia nigra pars compacta (SNpc). Then, oxidative metabolism was studied 24h and 7 days later in SNpc and corpus striatum (CS). Tyrosine hydroxylase and GFAP immunohistochemistry assays were carried out at 7 days. In addition, animals were evaluated in open field, adhesive removal, staircase and traverse beam tests. Glutathione depletion induced compensatory response in catalase activity and glial response in the in SNpc and no oxidative damage was observed. However, a loss in dopaminergic cells was found. At the same time, animals with glutathione depletion have shown poor performance in behavioral tests except for staircase test. These results suggest that glutathione depletion can be related to sensory-motor dysfunction.
authors.affiliation: International Center for Neurological Restoration, Havana, Cuba. Electronic address: mldiaz@neuro.ciren.cu.
authors.forename: Mei-Li
authors.initials: ML
authors.lastname: Díaz-Hung
authors.affiliation: International Center for Neurological Restoration, Havana, Cuba.
authors.forename: Lisette
authors.initials: L
authors.lastname: Blanco
authors.affiliation: International Center for Neurological Restoration, Havana, Cuba.
authors.forename: Nancy
authors.initials: N
authors.lastname: Pavón
authors.affiliation: International Center for Neurological Restoration, Havana, Cuba.
authors.forename: Rilda
authors.initials: R
authors.lastname: León
authors.affiliation: International Center for Neurological Restoration, Havana, Cuba.
authors.forename: Bárbara
authors.initials: B
authors.lastname: Estupiñan
authors.affiliation: International Center for Neurological Restoration, Havana, Cuba.
authors.forename: Eduardo
authors.initials: E
authors.lastname: Orta
authors.affiliation: Faculty of Biology, University of Havana, Cuba.
authors.forename: Klaudia
authors.initials: K
authors.lastname: Martínez
authors.affiliation: International Center for Neurological Restoration, Havana, Cuba.
authors.forename: Isabel
authors.initials: I
authors.lastname: Fernández
mesh_terms: D000818:Animals; D019328:Buthionine Sulfoximine / Q000633:toxicity*; D003342:Corpus Striatum / Q000378:metabolism; D059290:Dopaminergic Neurons / Q000187:drug effects / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism*; D008124:Locomotion / Q000187:drug effects; D008297:Male; D008845:Microinjections; D009043:Motor Activity / Q000187:drug effects; D065842:Pars Compacta / Q000378:metabolism*; D011597:Psychomotor Performance / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: D005904:Glial Fibrillary Acidic Protein; D019328:Buthionine Sulfoximine; D014446:Tyrosine 3-Monooxygenase; D005978:Glutathione
keywords: Antioxidant enzymes; Astrocytes; Dopaminergic cell; Glutathione; Malondialdehyde; Sensory-motor function