GM1 ganglioslde restores dopaminergic neurochemical and morphological markers in aged rats

Citation
Vm. Goettl et al., GM1 ganglioslde restores dopaminergic neurochemical and morphological markers in aged rats, NEUROSCIENC, 92(3), 1999, pp. 991-1000
Citations number
60
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROSCIENCE
ISSN journal
0306-4522 → ACNP
Volume
92
Issue
3
Year of publication
1999
Pages
991 - 1000
Database
ISI
SICI code
0306-4522(1999)92:3<991:GGRDNA>2.0.ZU;2-U
Abstract
The monosialoganglioside GM1 exerts neurotrophic-like activity in vitro and in vivo. In particular, it improves cholinergic neuron morphology and chem istry and learning abilities of cognitively impaired aged rats and young an imals with cholinergic lesions, and restores neurochemical, pharmacological , morphological and behavioral parameters in animal models of Parkinson's d isease. Our studies present evidence that GM1 reverses dopaminergic deficit s in the nigrostriatal neurons of aged rats. GM1 administered to aged Sprag ue-Dawley rats for 30 days reversed the decreased activity of tyrosine hydr oxylase in the midbrain and striatum, elevated the reduced protein content and mRNA levels of the enzyme in the midbrain, and reversed the decrements of dopamine and 3,4-dihydroxyphenylacetic acid content in both the midbrain and striatum. Tyrosine hydroxylase activity of the midbrain, but not of th e striatum, remained elevated for 15 days after discontinuing GM1. The coun t profiles of tyrosine hydroxylase-immunopositive neurons, the size of tyro sine hydroxylase-immunopositive neurons and the number of tyrosine hydroxyl ase-immunopositive fibers were decreased in the substantia nigra pars compa cta and the ventral tegmental area of aged rats. GM1 corrected the morpholo gy of dopaminergic neurons in the substantia nigra pars compacta and partia lly improved it in the ventral tegmental area. These findings support the notion that the aged striatal dopaminergic neuro ns respond to GM1, and strengthen the utility of using this compound for co mbating age-associated neuronal deficits. (C) 1999 IBRO. Published by Elsev ier Science Ltd.