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松鼠猴(Saimiri scireus)运动皮层中蛋白质营养不良引起的脂褐素积累的可逆性。

Reversibility of lipofuscin accumulation caused by protein malnutrition in the motor cortex of squirrel monkeys, Saimiri scireus.

作者信息

Manocha S L, Sharma S P

出版信息

Acta Histochem. 1977;58(2):219-31. doi: 10.1016/S0065-1281(77)80132-3.

Abstract

Lipofuscin pigment has been demonstrated histochemically in the motor cortex by the use of several histochemical and cytochemical methods in the healthy (maintained on a diet with 25% protein content) and protein malnourished (maintained on a diet with 2% protein content) adult animals. 4 animals in the latter category were rehabilitated over a period of 11 months and various histochemical techniques were repeated on the motor cortex of these animals. The healthy animals showed a somewhat uniform distribution of lipofuscin pigment in the neuronal perikarya with the perineuronal glia showing only slight occurrence of pigment bodies. The malnourished animals exhibited a significantly larger number of lipofuscin bodies in the neuronal as well as glial perikarya. The neurons, especially, showed aggregations of lipofuscin bodies characterized by a large increase in the activity of acid phosphatase and simple esterases. The rehabilitated animals, however, showed a decrease of lipofuscin pigment in the neuronal perikarya with a concomitant loss of lysosomal enzymes, while a significant increase of these bodies was observed in the perineuronal glial cells. It is evident that the formation of lipofuscin pigment gets accelerated under the extrinsic influence of dietary protein deprivation in the adult animals, but the process is reversed at least to some extent by halting the dietary deficiency or its correction by rehabilitation. The perineuronal glial cells appear to play a significant role in the removal of lipofuscin bodies from the neuronal perikarya. The significance of these observations has been discussed.

摘要

通过多种组织化学和细胞化学方法,在健康(以含25%蛋白质的饮食饲养)和蛋白质营养不良(以含2%蛋白质的饮食饲养)的成年动物的运动皮层中,已通过组织化学方法证实了脂褐素色素的存在。后一组中的4只动物经过11个月的康复期,对这些动物的运动皮层重复进行了各种组织化学技术检测。健康动物的神经元胞体中脂褐素色素分布较为均匀,神经周胶质细胞中仅偶尔出现色素体。营养不良的动物在神经元和胶质细胞的胞体中表现出大量明显更多的脂褐素小体。尤其是神经元,显示出脂褐素小体聚集,其特征是酸性磷酸酶和简单酯酶的活性大幅增加。然而,康复后的动物神经元胞体中的脂褐素色素减少,同时溶酶体酶丧失,而在神经周胶质细胞中观察到这些小体显著增加。显然,在成年动物中,饮食蛋白质缺乏的外在影响会加速脂褐素色素的形成,但通过停止饮食缺乏或通过康复纠正缺乏,这一过程至少在一定程度上会逆转。神经周胶质细胞似乎在从神经元胞体中清除脂褐素小体方面发挥着重要作用。已对这些观察结果的意义进行了讨论。

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