Fusco M, Donà M, Tessari F, Hallman H, Jonsson G, Gorio A
J Neurosci Res. 1986;15(4):467-79. doi: 10.1002/jnr.490150404.
The effect of exogenous monosialoganglioside GM1 on neurotoxin-induced lesioning of bulbo-spinal serotonergic neurons of newborn rats was studied by means of biochemical and immunocytochemical techniques. 5,7-dihydroxytryptamine (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. GM1 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 GM1 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 GM1 may have a preventing action on retrograde degenerative processes following chemical lesion and/or a growth-stimulating effect on injured 5-HT neurons.
采用生化和免疫细胞化学技术，研究了外源性单唾液酸神经节苷脂GM1对神经毒素诱导的新生大鼠延髓-脊髓5-羟色胺能神经元损伤的影响。用5,7-二羟基色胺（5,7-HT，一种选择性5-羟色胺神经毒素）处理新生大鼠，导致胸段和腰段脊髓中5-羟色胺（5-HT）和5-羟吲哚乙酸（5-HIAA）水平显著降低，而在脑桥延髓中5-HT和5-HIAA水平升高。这些生化改变与通过图像分析所分析的5-HT神经终末密度的类似变化在区域上相关。给予GM1（30mg/kg，连续4天）可拮抗5,7-HT处理诱导的2月龄大鼠腰段脊髓中5-HT和5-HIAA水平的降低，以及1月龄和2月龄大鼠胸段和腰段脊髓中5-HT神经终末密度的降低。在脑桥延髓中发现GM1有轻微的拮抗作用，神经毒素在该部位诱导5-HT和5-HIAA水平升高。这些数据支持这样的假说，即GM1可能对化学损伤后的逆行性变性过程具有预防作用和/或对受损的5-HT神经元具有生长刺激作用。
