The functional recovery of damaged brain: the effect of GM1 monosialoganglioside

• Published in: Journal of neuroscience research Vol. 12; no. 2-3; p. 397
• Main Authors: Toffano, G, Savoini, G, Aporti, F, Calzolari, S, Consolazione, A, Maura, G, Marchi, M, Raiteri, M, Agnati, L F
• Format: Journal Article
• Language: English
• Published: United States 1984
• Subjects: Animals; Brain Diseases - drug therapy; Brain Diseases - metabolism; Corpus Striatum - metabolism; Dopamine - metabolism; Electrophysiology; G(M1) Ganglioside - therapeutic use; Gangliosides - therapeutic use; Rats; Rats, Inbred Strains; Substantia Nigra; Synaptosomes - metabolism; Tyrosine 3-Monooxygenase - metabolism
• ISSN: 0360-4012
• DOI: 10.1002/jnr.490120224

In the present study the topology and the biochemical mechanisms underlying the functional recovery of the dopaminergic nigrostriatal system is further analyzed. Rats with unilateral hemitransection were treated with 30 mg/kg GM1 monosialoganglioside or with its internal ester derivative for different periods of time. GM1 enhances 3H-dopamine uptake in striatal synaptosomes of the lesioned side, and the enhancement of dopamine uptake precedes that of striatal tyrosine hydroxylase activity. The above biochemical effects are accompanied by changes in behavioral- and electrophysiological-related parameters. The effect of GM1 on striatal tyrosine hydroxylase of the lesioned side disappears when the ascending dopaminergic fibers are extensively lesioned. This suggests that the source of regrowing dopaminergic nerve terminals in the striatum of partially lesioned rats resides mainly in the intact axons remaining in the ipsilateral side. When GM1 is injected into partially lesioned rats kept in darkness, no effect on tyrosine hydroxylase activity is observed. This indicates that the mechanism through which GM1 acts involves a normal light-dark cycle.