SPROUTING OF STRIATAL SEROTONIN NERVE-TERMINALS FOLLOWING SELECTIVE LESIONS OF NIGRO-STRIATAL DOPAMINE NEURONS IN NEONATAL RAT
SPROUTING OF STRIATAL SEROTONIN NERVE-TERMINALS FOLLOWING SELECTIVE LESIONS OF NIGRO-STRIATAL DOPAMINE NEURONS IN NEONATAL RAT
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DOI：
10.1016/0361-9230(87)90092-x
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发表时间：
1987-08-01
影响因子：
3.8
通讯作者：
JONSSON, G
中科院分区：
文献类型：
--
作者：
LUTHMAN, J;BOLIOLI, B;JONSSON, G
新生儿脑池内6-羟基多巴胺（6-OHDA; 50 μ g）处理对大鼠纹状体5-羟色胺（5-HT）神经末梢的作用已经使用组织化学和神经化学方法表征。6-OHDA损伤导致纹状体多巴胺（DA）浓度降低60%，而5-HT水平增加约40%，体外3 H-5-HT摄取增加约60%。使用计算机图像分析，5-HT样免疫反应终末密度显着增加，发现在吻侧（+200%）和尾侧（+50%）纹状体。预处理与DA吸收阻滞剂amfolenic酸完全抵消了6-OHDA诱导的纹状体DA和5-HT神经元的变化，而预处理与去甲肾上腺素吸收阻滞剂地昔帕明没有显着的效果。新生儿6-OHDA治疗或地昔帕明+ 6-OHDA联合治疗后CNS中5-HT水平的区域分析显示，除观察到纹状体中5-HT增加外，对任何分析的脑区均无显著影响。进一步观察到纹状体5-羟基吲哚乙酸（5-HIAA）/5-HT比值降低，而3，4-二羟基苯乙酸（DOPAC）/DA比值升高，表明递质转换的代偿机制。这些变化完全逆转后，预处理与amfolenic酸。本研究结果支持了新生儿6-OHDA处理后的5-HT高神经支配是由纹状体DA神经元损伤引起的侧支出芽反应的观点。
The effects of neonatal intracisternal 6-hydroxydopamine (6-OHDA; 50 .mu.g) treatment on striatal serotonin (5-HT) nerve terminals in rat have been characterized using histo- and neurochemical methods. The 6-OHDA lesion caused a 60% reduction of striatal dopamine (DA) concentration when analyzed in the adult stage, while 5-HT levels were increased by about 40% and 3H-5-HT uptake in vitro was increased by about 60%. Using computerized image analysis, a marked increase in 5-HT-like immunoreactive terminal density was found in both rostral (+200%) and caudal (+50%) striatum. Pretreatment with the DA uptake blocker amfolenic acid completely counteracted the 6-OHDA-induced alterations in both DA and 5-HT neurons in the striatum, while pretreatment with the noradrenaline uptake blocker desipramine had no significant effects. Regional analysis of 5-HT levels in the CNS after neonatal 6-OHDA treatment or the combined desipramine + 6-OHDA treatment showed no significant effect in any of the brain areas analyzed, apart from the observed 5-HT increase in striatum. It was furthermore observed that the striatal 5-hydroxyindoleacetic acid (5-HIAA)/5-HT ratio was decreased, while the 3,4-dihydroxyphenylacetic acid (DOPAC)/DA ratio was increased following the 6-OHDA lesion, indicating compensatory mechanisms in turnover of transmitters. These alterations were completely reversed after pretreatment with amfolenic acid. The present results support the view that the 5-HT hyperinnervation following neonatal 6-OHDA treatment is a collateral sprouting response induced by lesioning of the striatal DA neurons.