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目的探讨锰中毒性帕金森综合征大鼠中枢多巴胺能神经元缺失与行为学改变之间的关系。方法将40只大鼠随机分成对照组、染锰组,分别腹腔注射生理盐水和Mn Cl2溶液,第16周进行4项行为学测试。行为学测试后,测试脑锰含量,酪氨酸羟化酶(Tyrosine Hydroxylase,TH)可反映黑质内多巴胺能神经元数量,故对两组大鼠的黑质、纹状体、海马进行酪氨酸羟化酶免疫组织化学染色。结果染锰组大鼠出现学习记忆力下降、动作迟缓、肌张力增高、平衡功能障碍等行为学改变;染锰组大鼠脑锰含量(4.578±1.281,ug/g)高于对照组(0.610±0.251,ug/g),t=-9.611,P<0.001;与对照组相比,染锰组黑质(0.001±0.004)TH阳性表达量减少,t=9.988,P<0.001;染锰组纹状体(0.016±0.007)TH阳性表达量减少,t=11.089,P<0.001;染锰组海马(0.008±0.002)TH阳性表达量减少,t=15.023,P<0.001。结论锰中毒性帕金森综合征大鼠中脑-边缘系统和中脑-皮质系统的多巴胺能神经元损害可能是智能减退、运动障碍等高级神经活动异常的生化基础。
Objective To investigate the relationship between the loss of central dopaminergic neurons and behavioral changes in manganese-toxic Parkinsonism rats. Methods Forty rats were randomly divided into control group, manganese group, intraperitoneal injection of normal saline and MnCl2 solution, and four behavioral tests at the 16th week. Behavioral tests, the test of brain manganese content, tyrosine hydroxylase (Tyrosine Hydroxylase, TH) reflect the number of dopaminergic neurons in the substantia nigra, so the two groups of rats in the substantia nigra, striatum, hippocampus cheese Hydroxylase Immunohistochemical Staining. Results The rats with manganese exposure had behavioral changes such as decreased learning and memory abilities, slowed movement, increased muscle tone, and balance dysfunction. Manganese levels in manganese-exposed rats (4.578 ± 1.281, ug / g) were significantly higher than those in control rats 0.251, ug / g), t = -9.611, P <0.001. Compared with the control group, the positive expression of TH (+0.00 ± 0.004) T = 11.089, P <0.001. The positive expression of TH in the hippocampus (0.008 ± 0.002) in the manganese group decreased (t = 15.023, P <0.001). Conclusion The damage of dopaminergic neurons in mesencephalic-limbic system and midbrain-cortex system of rats with toxic Parkinsonism may be the biochemical basis of abnormal high level neural activity such as dementia and dyskinesia.