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本实验以饮用高氟水（１００ｐｐｍ）的方法制造了雄性大鼠慢性氟中毒模型。对脑干中缝背核神经元进行了光、电镜观察及５－ＨＴ能神经元的免疫细胞化学定性、定量研究。结果表明：氟中毒大鼠中缝背核神经元的核浆比值大，核内异染色质增多且边集。线粒体扩张、嵴断裂或消失。粗面内质网池、高尔基复合体扁平囊亦扩张。脂褐素增多，并有较多的自噬体；免疫细胞化学显示，氟中毒大鼠中缝背核５－ＨＴ能神经元胞质内５－ＨＴ阳性反应颗粒减少且界限不清，显微图象分析仪检测上述神经元内５－ＨＴ含量明显降低。这些结果提示：高氟摄入对中枢５－ＨＴ能神经元有直接损害、对其５－ＨＴ的产生有抑制作用。
In this experiment, a model of chronic fluorosis in male rats was made by drinking high fluoride water (100ppm). The brainstem dorsal raphe nucleus neurons were observed by light and electron microscopy and 5-HT neuron immunocytochemistry qualitative and quantitative study. The results showed that the ratio of nucleus to plasma of dorsal raphe nucleus neurons in fluorosis rats was increased, heterochromatin in the nucleus increased and marginal set was observed. Mitochondria dilate, cristae break or disappear. Rough endoplasmic reticulum pool, Golgi complex flat capsule also dilated. Lipofuscin increased, and more autophagosomes; immunocytochemistry showed that fluoridated rat dorsal raphe nucleus 5-HT neuronal cytoplasmic 5-HT-positive particles decreased and unclear boundaries, micrograph As analyzed by the analyzer, the 5-HT content in the neurons was significantly reduced. These results suggest that high fluoride intake directly damages central 5-HT neurons and inhibits 5-HT production.