Chronic GM1 ganglioside treatment reduces dopamine cell body degeneration in the substantia nigra after unilateral hemitransection in rat.
The effect of GM1 ganglioside on the recovery of dopaminergic nigro-striatal neurons was studied in rats after unilateral hemitransection. GM1 treatment partially prevented the decrease of tyrosine hydroxylase (TH) activity caused by hemitransection in the substantia nigra ipsilateral to the lesion. Concomitantly a significant increase of TH-immunoreactivity in the substantia nigra was also detected. In particular, chronic treatment with GM1 prevented the disappearance of TH-positive cell bodies in the substantia nigra and induced the appearance of longer TH-positive dendrites with respect to the saline treatment. These data indicate that GM1 treatment maintains the number of dopaminergic cell bodies in the substantia nigra after hemitransection by protecting against retrograde neuronal degeneration.
D000818:Animals; D003342:Corpus Striatum / Q000187:drug effects; D004292:Dominance, Cerebral / Q000187:drug effects*; D004298:Dopamine / Q000378:metabolism; D005677:G(M1) Ganglioside / Q000494:pharmacology*; D005732:Gangliosides / Q000494:pharmacology*; D005904:Glial Fibrillary Acidic Protein; D007381:Intermediate Filament Proteins / Q000378:metabolism; D009410:Nerve Degeneration / Q000187:drug effects*; D009416:Nerve Regeneration / Q000187:drug effects*; D009434:Neural Pathways / Q000187:drug effects; D009474:Neurons / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000187:drug effects*; D013378:Substantia Nigra / Q000187:drug effects*; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
D005732:Gangliosides; D005904:Glial Fibrillary Acidic Protein; D007381:Intermediate Filament Proteins; D011954:Receptors, Dopamine; D005677:G(M1) Ganglioside; D014446:Tyrosine 3-Monooxygenase; D004298:Dopamine