CHANGES IN CENTRAL NORADRENALINE NEURONSADMINISTRATION AFTER SYSTEMIC 6‐HYDROXYDOPAMINE ADMINISTRATION
CHANGES IN CENTRAL NORADRENALINE NEURONSADMINISTRATION AFTER SYSTEMIC 6‐HYDROXYDOPAMINE ADMINISTRATION
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全身 6-羟基多巴胺给药后中枢去甲肾上腺素神经元给药的变化
DOI：
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发表时间：
1973
期刊：
影响因子：
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通讯作者：
G. Jonsson
中科院分区：
文献类型：
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作者：
C. Sachs;G. Jonsson
- 向成年大鼠静脉注射大剂量6-羟基多巴胺（100 mg/kg）导致大脑皮层和脊髓中[3 H]NA的体外摄取显著且持久地减少（约30%），而下丘脑中未见变化。全脑的内源性NA也同样减少（约20%）。荧光组织化学显示，在神经支配大脑皮层的背侧NA束轴突中，6-羟基多巴胺诱导了儿茶酚胺蓄积，这是退行性体征。得出结论，成年大鼠的血脑屏障对于全身注射6-羟基多巴胺的神经毒性作用并不完全具有保护作用，6-羟基多巴胺可导致大脑皮层和脊髓中大量NA神经末梢变性。先前的研究表明，由于血脑屏障发育不完全，在出生后1周内全身注射6-羟基多巴胺会导致大量中枢NA神经末梢永久性和选择性变性。6-羟基多巴胺的这种屏障在出生后第7天和第9天之间形成（Sachs，1973）。在本研究中，发现6-羟基多巴胺导致9至28日龄大鼠大脑皮层中[3 H]NA摄取的短暂性小幅减少，而在老年大鼠中，6-羟基多巴胺产生的损伤是持久的。因此，上升到大脑皮层的NA神经似乎具有再生能力，可以在出生后约28天内对6-羟基多巴胺诱导的变性进行再生，但随后消失或明显延迟。
—Intravenous injection of a large dose of 6‐hydroxydopamine (100 mg/kg) to adult rats caused a significant and long‐lasting reduction (about 30 per cent) of the in oirro uptake of [3H]NA in the cerebral cortex and spinal cord, while no changes were seen in the hypothalamus. The endogenous NA in whole brain was similarly reduced (about 20 per cent). Fluorescence histochemistry revealed catecholamine accumulations which are degenerative signs, induced by 6‐hydroxydopamine, in axons of the dorsal NA bundle innervating the cerebral cortex. It is concluded that the blood–brain barrier in adult rats is not completely protective with respect to the neurotoxic action of systemically injected 6‐hydroxydopamine, which can produce degeneration of a significant number of NA nerve terminals in the cerebral cortex and spinal cord. Previous studies have shown that 6‐hydroxydopamine caused a permanent and selective degeneration of a large number of central NA nerve terminals when injected systemically up to 1 week after birth, due to an incompletely developed blood‐brain barrier. This barrier for 6‐hydroxydopamine develops between the 7th and 9th day after birth (Sachs, 1973). In the present study 6‐hydroxydopamine was found to cause a small transient reduction in [3H]NA uptake in cerebral cortex of rats between 9 and 28 days of age, while in older rats the damage produced by 6‐hydroxydopamine was long‐lasting. Thus, the NA nerves ascending to the cerebral cortex seem to possess a regenerative capacity to a 6‐hydroxydopamine‐induced degeneration up to about 28 days postnatally, but which later disappears or is markedly retarded.