Nwanze E, Jonsson G
Neurosci Lett. 1981 Oct 23;26(2):163-8. doi: 10.1016/0304-3940(81)90343-8.
Continuous administration of D-amphetamine to mice by osmotic minipumps (placed s.c.) delivering 25 micrograms/h for 7 days led to significant decreases in the endogenous dopamine concentration (-51%) and [3H]noradrenaline uptake (-43%) in vitro in the caudate nucleus. Fluorescence histochemical analysis demonstrated a marked reduction of dopamine fluorescence as well as catecholamine accumulations (sign of neurotoxicity) in the caudate nucleus. No notable effects were noted on the fluorescence morphology of the dopamine cell bodies in the mesencephalon. The dopamine levels were still significantly reduced (-37%) after two months, while the [3H]noradrenaline uptake had at this time-point reached almost normal values. The results are compatible with the view that D-amphetamine can induce acutely a neurodegenerative damage of central dopamine neurons at the level of the nerve terminals in the caudate nucleus with possibilities for regeneration and recovery in the chronic state.
通过皮下植入的渗透微型泵以每小时25微克的剂量持续7天给小鼠注射D-苯丙胺，导致尾状核中内源性多巴胺浓度显著降低（-51%），体外[3H]去甲肾上腺素摄取显著降低（-43%）。荧光组织化学分析表明，尾状核中多巴胺荧光以及儿茶酚胺积累（神经毒性迹象）明显减少。中脑中多巴胺细胞体的荧光形态未观察到明显影响。两个月后多巴胺水平仍显著降低（-37%），而此时[3H]去甲肾上腺素摄取已接近正常水平。这些结果与以下观点一致，即D-苯丙胺可在尾状核神经末梢水平急性诱导中枢多巴胺神经元的神经退行性损伤，在慢性状态下有再生和恢复的可能。
