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新生大鼠多巴胺耗竭性损伤诱导的纹状体神经肽Y免疫反应性增加,可被纹状体内富含多巴胺的移植所逆转。

The increase in striatal neuropeptide Y immunoreactivity induced by neonatal dopamine-depleting lesions in rats is reversed by intrastriatal dopamine-rich transplants.

作者信息

Abrous D N, Le Moal M, Herman J P

机构信息

INSERM U-259, Université Bordeaux II, France.

出版信息

Brain Res. 1994 Sep 5;656(1):169-73. doi: 10.1016/0006-8993(94)91379-x.

Abstract

The aim of the present experiment was to test whether: (i) the destruction of the dopaminergic meso-telencephalic pathway in neonatal rats induces an increase in the density of Neuropeptide Y immunoreactive (NPY-IR) neuronal perikarya within the denervated neostriatum; (ii) embryonic dopaminergic neurons grafted into the neonatal neostriatum could block such an effect of the lesion. As a control, density of NPY-IR neurones was also examined in rats lesioned and/or grafted at adulthood. The ascending dopaminergic system of 3-day-old rat pups or adult rats was unilaterally lesioned by intrahypothalamic injection of 6-hydroxydopamine. Grafting was performed six days later. The neonatal lesion increased the number of NPY-IR neurones on the lesioned side by 24% as compared to the contralateral neonstriatum. This increase was abolished in the neostriatum bearing dopaminergic grafts as evaluated six weeks after grafting. These effects are similar to that observed in animals lesioned and/or grafted as adults and further extend the range of post-lesion modifications which can be reversed by the implantation of embryonic DA neurones to neonates.

摘要

本实验的目的是测试

(i)新生大鼠中多巴胺能中脑-端脑通路的破坏是否会导致去神经支配的新纹状体内神经肽Y免疫反应性(NPY-IR)神经元胞体密度增加;(ii)移植到新生大鼠新纹状体内的胚胎多巴胺能神经元是否可以阻止损伤的这种效应。作为对照,还检查了成年期损伤和/或移植的大鼠中NPY-IR神经元的密度。通过下丘脑内注射6-羟基多巴胺对3日龄幼鼠或成年大鼠的上行多巴胺能系统进行单侧损伤。六天后进行移植。与对侧新纹状体相比,新生期损伤使损伤侧NPY-IR神经元的数量增加了24%。移植六周后评估发现,在植入多巴胺能移植物的新纹状体中,这种增加被消除。这些效应与在成年期损伤和/或移植的动物中观察到的效应相似,并进一步扩展了损伤后可通过向新生动物植入胚胎多巴胺能神经元而逆转的改变范围。

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