Gangliosides in rabbit and human skeletal muscle with denervation atrophy.

In experimental denervation of rabbit skeletal muscle, an increase of gangliosides has been reported. Ganglioside, DNA, total lipid and protein levels were studied in experimental denervation of rabbit gastrocnemius muscle and in human skeletal muscle with denervation atrophy. In severe human denervation atrophy total ganglioside, DNA and total lipid levels were increased, and protein levels decreased as compared with controls. The ganglioside pattern was changed in severe human denervation atrophy and showed a significant increase of a GT1b-like and moderate decrease of a GM1-like compound. Findings in experimentally denervated rabbit muscle resembled results obtained in human denervation atrophy, showing a significant increase of total ganglioside levels as well as a moderate increase of GT1b-like and decrease of GM1-like compounds.

Neurochemical investigations of aged human brain cortex.

Neurochemical investigation of FC and TC of 10 brains of old age and 10 controls did not reveal significant differences of total ganglioside, DNA, protein, and lipid levels. With regard to individual gangliosides there was a significant decrease of the percentage of GM1 in the FC and a significant decrease of GM1, GD1a, GM2 as well as a significant increase of GD1b and GD3 in the TC of the aged brains. Our results present some neurochemical evidence for regionally different changes in neuronal processes in the aged human brain, whereas neuronal cell loss might play only a minor role in this condition.

Striatal ganglioside levels in the rat following kainic acid lesions: comparison with Huntington's disease.

Ganglioside and DNA levels were estimated in the striatum of rats 10 days and 6 weeks after lesioning by intrastriatal injection of kainic acid. There was a moderate, 21-24% decrease of the ganglioside concentration per unit protein on the side of the lesion, which can be ascribed to the loss of the intrinsic striatal neurons following the injection of kainic acid. On the other hand, there was a 131 and 60% increase of DNA per unit protein in the kainate injected side 10 days and 6 weeks after the lesions, respectively; these changes apparently reflected the gliotic reaction brought about by the neurotoxin. Qualitatively similar findings--a decrease of ganglioside and an increase of DNA levels per unit protein--were also found in the brain of patients with Huntington's disease; however, as compared with the corresponding control material, the decrease of the ganglioside concentration was more pronounced in the striatum of Huntington's disease (by 38% in the caudate nucleus and by 46% in the putamen) than in the kainate lesioned rat striatum. This difference could be due to the different proportions of the intrinsic and extrinsic neuronal plasma membranes in the striatum of the two species; however, the possibility of a more generalized affection of neuronal plasma membranes in Huntington's disease may also be envisaged.