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GM 1 ganglioside counteracts selective neurotoxin‐induced lesion of developing serotonin neurons in rat spinal cord
Author(s) -
Fusco M.,
Donà M.,
Tessari F.,
Hallman H.,
Jonsson G.,
Gorio A.
Publication year - 1986
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490150404
Subject(s) - neurotoxin , spinal cord , ganglioside , serotonin , neuroscience , lesion , chemistry , medicine , biology , pathology , biochemistry , receptor
The effect of exogenous monosialo ganglioside GM 1 on neurotoxin‐induced lesioning of bulbo‐spinal serotonergic neurons of newborn rats was studied by means of biochemical and immunocytochemical techniques. 5,7‐dihydroxytrypatamine (5,7‐HT, a selective serotonin neurotoxin) treatment of newborn rats caused a pronounced reduction of 5‐hydroxytryptamine (5‐HT) and 5‐hydroxyindoleacetic acid (5‐HIAA) levels in the thoracic and lumbar spinal cord, while an increase of 5‐HT and 5‐HIAA was found in the pons medulla. These biochemical alterations were regionally correlated with similar changes in 5‐HT nerve terminal density analyzed by image analysis. GM 1 administration (30 mg/kg for 4 consecutive days) antagonized the reduction of 5‐HT and 5‐HIAA levels induced by 5, 7‐HT treatment in the lumbar spinal cord of 2‐month‐old rats, as well as the decrease of 5‐HT nerve terminal density in both thoracic and lumbar spinal cord of 1‐ and 2‐month‐old rats. A minor counteracting effect of GM 1 was found in the pons medulla where the neurotoxin induced an increase of 5‐HT and 5‐HIAA levels. These data support the hypothesis that GM 1 may have a preventing action on retrograde degenerative processes following chemical lesion and/or a growth‐stimulating effect on injured 5‐HT neurons.