MANGANESE-INDUCED BEHAVIORAL DYSFUNCTION AND ITS NEUROCHEMICAL MECHANISM IN GROWING MICE
MANGANESE-INDUCED BEHAVIORAL DYSFUNCTION AND ITS NEUROCHEMICAL MECHANISM IN GROWING MICE
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DOI：
10.1111/j.1471-4159.1979.tb05267.x
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发表时间：
1979-01-01
影响因子：
4.7
通讯作者：
SAXENA, DK
中科院分区：
文献类型：
--
作者：
CHANDRA, SV;SHUKLA, GS;SAXENA, DK
哺乳小鼠从出生时就间接通过母亲接触到锰，然后在断奶后直接通过饮用水接触到锰。这些小鼠的生长发育与同龄对照组几乎完全相同。每隔30天测量一次后代的运动活动，与对照组相比，锰处理小鼠在第60天和第90天的运动活动显著增加。运动活动的增加与治疗小鼠纹状体中多巴胺和去甲肾上腺素水平的显著升高有关。锰暴露后小鼠纹状体酪氨酸、同型香草酸和锰的水平也显著升高。我们建立了早期Mg中毒动物模型，推测纹状体胺可能在Mg中毒小鼠行为功能障碍的产生中起作用。这些发现的含义讨论了与早期工业锰中毒的精神阶段的表现在人。
Suckling mice were exposed to Mn from birth indirectly through their mothers and then directly through drinking water after weaning. The growth and development of these mice and their age-matched controls were almost identical. Motor activity of offspring measured at 30 day intervals showed a significant increase at 60 and 90 days in Mn-treated mice compared to controls. Increased motor activity was associated with significant elevation in the levels of dopamine and norepinephrine in the corpus striatum of treated mice. The levels of striatal tyrosine, homovanillic acid and Mn were also significantly increased in mice after Mn exposure. An animal model of early Mg poisoning was developed with a possible role of striatal amines in the production of behavioral dysfunction in the treated mice. Implications of these findings are discussed in relation to the manifestations of the psychiatric phase of early industrial Mn poisoning in man.