用神经毒素辣椒素治疗新生大鼠后脊髓丘脑束神经元的丧失。

S Saporta
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引用次数: 14

摘要

本实验的目的是确定成年大鼠的脊髓丘脑束(STT)细胞的组织是否在其大部分小直径外周传入纤维丢失后发生改变,这是由于新生儿给药辣椒素造成的。在出生后第1、2、7、15天,将大鼠幼崽随机分为正常对照组、对照对照组和皮下注射辣椒素(50 mg/kg)组;或者在PND 1 3 5注射。60 d时麻醉,在中央外侧核(CL)、后核(PO)和腹底复合体(VB)区域或CL或VB区域注射0.1微升的小麦胚芽凝集素结合的辣根过氧化物酶(WGA:HRP)。存活48小时后,灌注动物,用四甲基联苯胺观察神经元HRP反应产物。WGA: hrp标记的STT神经元数量和分布随辣椒素注射时间的变化而变化。在PND 7日或之前注射辣椒素的大鼠显示脊髓浅层标记STT神经元的显著减少。此外,即使在PND 7之前接受大剂量丘脑注射,动物的I层神经元也未被标记。在PND 7和PND 15上注射辣椒素的动物,标记的STT神经元的分布没有差异,尽管PND 7动物的标记神经元数量有所减少。为了确定标记的STT神经元的缺失不是由于某些技术错误或WGA:HRP在注射部位的扩散不足,我们在PND 1和正常成年动物的丘脑中注射了6针WGA:HRP。在密集的反应产物核心没有延伸到尾侧后连合的地方,WGA: hrp阳性神经元的定位和分布与大丘脑注射所描述的病例相似。在PND 1动物丘脑注射的致密核延伸到中脑的地方,标记对侧脊髓固有核浅层和第一层的神经元。这些研究表明,成年大鼠在新生期接受神经毒素辣椒素治疗后,STT起源细胞的数量和分布发生了改变,而且这种影响仅限于关键的产后时期。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Loss of spinothalamic tract neurons following neonatal treatment of rats with the neurotoxin capsaicin.

The purpose of the present experiments was to determine whether the organization of spinothalamic tract (STT) cells of adult rats was altered following the loss of most of their small-diameter peripheral afferent fibers, resulting from the neonatal administration of capsaicin. Rat pups were randomly assigned to serve as normal controls, to serve as vehicle controls, or to receive subcutaneous injections of capsaicin (50 mg/kg) on postnatal day (PND) 1, 2, 7, or 15; or an injection on PND 1, 3, and 5. When 60 days old, they were anesthetized and received 0.1-microliter thalamic injections of wheatgerm agglutinin conjugated to horseradish peroxidase (WGA:HRP) in the area of the central lateral nucleus (CL), the posterior group (PO), and the ventrobasal complex (VB), or the area of CL or VB. Following a survival time of 48 hr, the animals were perfused, and neuronal HRP reaction product was visualized with tetramethylbenzidine. The number and distribution of WGA:HRP-labeled STT neurons varied in treated animals with the time of capsaicin injection. Rats injected with capsaicin on or before PND 7 demonstrated a significant reduction of labeled STT neurons from the superficial laminae of the spinal cord. Additionally, lamina I neurons were unlabeled in animals treated before PND 7 even with large thalamic injections. Differences in the distribution of labeled STT neurons could not be demonstrated for animals injected with capsaicin on PND 7 or PND 15, though there was a decrement in the number of labeled neurons in PND 7 animals. In order to make certain that absence of labeled STT neurons was not due to some technical error or to insufficient spread of WGA:HRP at the site of injection, six injections of WGA:HRP were placed in the thalamus of PND 1 and normal adult animals. Where the dense core of reaction product did not extend caudal to the posterior commissure, WGA:HRP-positive neurons were located and distributed similarly to those cases described for large thalamic injections. Neurons in superficial laminae of the nucleus proprius and lamina I of the contralateral spinal cord were labeled where the dense core of the thalamic injection extended into the mesencephalon of PND 1 animals. These studies indicate that the number and distribution of the cells of origin of the STT are altered in adult rats following their neonatal treatment with the neurotoxin capsaicin, and that this effect is limited to a critical postnatal period.

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