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中文摘要：
目的 探讨碘缺乏和碘过量对仔二代Wistar大鼠海马神经元特异性烯醇化酶（NSE）发育的影响。方法 按照饮用水含碘（KIO3）量不同，将大鼠随机分为6组（NI、5HI、10HI、50HI、100HI、LI），取1、20、60日龄仔二代鼠大脑，应用免疫组织化学技术观察海马CA3区神经元，并对NSE反应阳性细胞进行形态学计量分析。结果 1日龄：各组仔鼠大脑海马CA3区NSE阳性反应极微弱。20日龄：LI组NSE阳性细胞的细胞核直径、细胞体直径、面数密度和灰度值均比NI组明显减小（P〈0．05或〈0．01）；100HI组面数密度和灰度值小于NI组，差异亦有统计学意义（P〈0．05）。60日龄：与NI组比较，LI、100HI组NSE阳性细胞的细胞核直径、细胞体直径、核质比和面数密度均明显减小（P〈0．05或〈0．01）；LI、50HI、100HI组的NSE阳性细胞灰度值均比NI组明显降低（P〈0．05或〈0．01）。结论 碘缺乏和长期严重碘过量使仔二代大鼠大脑海马神经元NSE活性降低，影响神经元的能量代谢．其机制可能与碘缺乏和严重碘过量所致的甲状腺功能低下有关。
英文摘要：
Objective To study the effects of iodine deficiency or excess on the expression of neuron specific enolase（NSE） of hippocampal neurons in the second filial generation of Wistar rats. Methods The rats were divided into six groups （NI,5HI, 10HI,50HI, 100HI,LI） fed with water containing different dosage of iodine. The second filial generations of 1-day, 20-day and 60-day were observed of the morphology of the hippocampal neurons. The expression of NSE were examined by immunohistochemistry, the diameter of neurons, numerical density in the area and the average of gray scale were measured by image analysis. Results There were no significant changes observed in iodine deficiency and all excess groups at the age of 1-day in the second filial generation of rats compared with NI group. But on the 20th day, immunohistochemical staining and morphological image analysis of NSE positive neurons in hippocampus CA3 area indicated that the diameter, the numerical density in the area and the average of gray scale of neuron were reduced gradually in 100HI and LI groups compared with NI group （P 〈 0.05 or 〈 0.01 ）. With the prolongation of time, on the 60th day, the diameter, numerical density in the area and the average of grey scale of cerebral hippocampus neuron were further decreased, especially in 100HI and LI groups（P 〈 0.05 or 〈 0.01 ） ; furthermore, statically significance of gray scale was found in 50HI, 100HI and LI groups compared with the normal gruop（P 〈 0.05 or 〈 0.01 ）. Conclusions Both iodine deficiency and excess can affect the development and energy metabolism of hippocampal neurons in the second filial generation of Wistar rats, whose mechanism is perhaps related to hypothyroidism induced by iodine deficiency or excess.
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