Fusco M, Figliomeni B, Gorio A, Vantini G
Fidia Research Laboratories, Via Ponte della Fabbrica 3/A, 35031 Abano Terme, Italy.
Neurochem Int. 1988;13(2):251-9. doi: 10.1016/0197-0186(88)90062-9.
The postnatal development of serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in the pons medulla and spinal cord segments of rats treated with 5,7-dihydroxytryptamine (5,7-HT) and/or GM1 ganglioside has been investigated. Animals have been sacrificed at 4, 7, 28 and 56 days of age. In control rats, 5-HT and 5-HIAA increase in all areas during the first postnatal week. Thereafter, 5-HT and 5-HIAA remain constant in the thoracic and lumbar segments while a further increment takes place in the cervical portion. In the pons medulla, 5-HT reaches a plateau at 28 days, while 5-HIAA reaches a peak at 7 days and then declines to the adult value at 28 days. Neonatal administration of 5,7-HT produces mixed-type alterations in the developing bulbospinal serotoninergic system. Whilst 5-HT and 5-HIAA markedly decrease in the most distal 5-HT nerve terminal projections (thoracic and lumbar cord) they increase in the pons medulla ("pruning effect"). These alterations are accompanied by regional variations of the 5-HIAA/5-HT ratio, an index of 5-HT turnover. In particular, a prominent decrease of 5-HIAA/5-HT occurs in the lumbar segment of 1- and 2-month-old rats. In this area, where the effect of 5,7-HT is the most severe, an "up-regulation" of 5-HT, receptors is observed in 2-month-old rats. GM1 administration does not modify the development of the bulbospinal serotoninergic system. However, GM1 treatment has a counteracting effect on the alterations induced by 5,7-HT. Recovery of 5-HT and 5-HIAA levels occurs in the thoracic and lumbar cord of 1- and 2-month-old rats and is paralleled by a reduction of the "pruning effect" in the pons medulla. Furthermore, in the lumbar cord of 2-month-old rats, GM1 prevents the decrease of the 5-HIAA/5-HT ratio and the "up-regulation" of 5-HT(l) receptors induced by the neurotoxin. It is suggested that the GM1 effect is due to a prevention of the retrograde axonal degeneration occurring after the lesion and/or a growth stimulation of injured axons.
研究了用5,7 - 二羟基色胺（5,7 - HT）和/或GM1神经节苷脂处理的大鼠脑桥延髓和脊髓节段中5 - 羟色胺（5 - HT）和5 - 羟吲哚乙酸（5 - HIAA）的产后发育情况。在4、7、28和56日龄时处死动物。在对照大鼠中，产后第一周所有区域的5 - HT和5 - HIAA均增加。此后，胸段和腰段的5 - HT和5 - HIAA保持恒定，而颈段则进一步增加。在脑桥延髓，5 - HT在28天时达到平台期，而5 - HIAA在7天时达到峰值，然后在28天时降至成年值。新生期给予5,7 - HT会在发育中的延髓脊髓5 - 羟色胺能系统中产生混合型改变。虽然5 - HT和5 - HIAA在最远端的5 - HT神经终末投射（胸段和腰段脊髓）中显著减少，但在脑桥延髓中却增加（“修剪效应”）。这些改变伴随着5 - HIAA/5 - HT比值的区域差异，5 - HIAA/5 - HT比值是5 - HT周转的一个指标。特别是，1月龄和2月龄大鼠腰段的5 - HIAA/5 - HT显著降低。在这个5,7 - HT作用最严重的区域，2月龄大鼠中观察到5 - HT受体的“上调”。给予GM1不会改变延髓脊髓5 - 羟色胺能系统的发育。然而，GM1治疗对5,7 - HT诱导的改变有抵消作用。1月龄和2月龄大鼠胸段和腰段脊髓中5 - HT和5 - HIAA水平恢复，同时脑桥延髓中的“修剪效应”减弱。此外，在2月龄大鼠的腰段脊髓中，GM1可防止神经毒素诱导的5 - HIAA/5 - HT比值降低和5 - HT（1）受体的“上调”。提示GM1的作用是由于预防了损伤后发生的逆行性轴突退变和/或对受损轴突的生长刺激。
