Rebiére A, Dainat J
Exp Brain Res. 1976 Jul 28;25:511-27. doi: 10.1007/BF00239784.
The effects of neonatal hypothyroidism on synaptic organization, glial surrounding and cytoplasmic structures of the Purkinje cell perikaryon of the 21 days old rat were studied by electron microscopy. Hypothyroidism decreases the size of the perikaryon but does not change the nucleo-cytoplasmic ratio of the cell. At 21 days the axonal endings that make synapse on the Purkinje cell perikaryon, already show the adult morphological features and hypothyroidism does not change these. The general synaptic density on the Purkinje perikaryon is not significantly altered, but the cells of hypothyroid animals still recieve 1/3 of their axo-somatic synapses on somatic spines, whereas euthyroid animals have practically no synapses on somatic spines. Hypothyroidism leads the disappearance of the synchronism which normally exists between the translocation or resorption of the Purkinje cell somatic spines and the establishment of the basket cell synapses. The basket cell axons of the normal animals form synapses only on the smooth surfaces of the Purkinje cell perikaryon while they also establish it on the somatic spines of the hypothyroid animals. The density of the axon terminals of basket cells is decreased, while that of the endings of Purkinje cell axon collaterals and of climbing fibers are increased. Hypothyroidism produces an increase in the size of the glial sheath around the Purkinje perikaryon. It does not alter the proportion of the cytoplasmic area occupied by mitochondria, but in thyroid deficiency there is an increase in the numbers of mitochondria which are reduced in average size. The Golgi apparatus is only slightly affected. Thyroid defiency does not alter the density of the cytoplasmic agreggates of free ribosomes but there is a decrease in density of the ergastoplasm and a disorganization of the Nissl bodies.
通过电子显微镜研究了新生期甲状腺功能减退对21日龄大鼠浦肯野细胞胞体突触组织、胶质细胞环绕及细胞质结构的影响。甲状腺功能减退会减小胞体大小,但不会改变细胞的核质比。在21日龄时,与浦肯野细胞胞体形成突触的轴突终末已呈现成年形态特征,甲状腺功能减退不会改变这些特征。浦肯野细胞胞体上的总体突触密度无显著改变,但甲状腺功能减退动物的细胞仍有1/3的轴-体突触位于体细胞棘上,而甲状腺功能正常的动物在体细胞棘上几乎没有突触。甲状腺功能减退导致浦肯野细胞体细胞棘的移位或吸收与篮状细胞突触建立之间通常存在的同步性消失。正常动物的篮状细胞轴突仅在浦肯野细胞胞体的光滑表面形成突触,而在甲状腺功能减退动物的体细胞棘上也会形成突触。篮状细胞轴突终末的密度降低,而浦肯野细胞轴突侧支和攀缘纤维终末的密度增加。甲状腺功能减退会使浦肯野细胞胞体周围的胶质鞘增大。它不会改变线粒体所占细胞质面积的比例,但在甲状腺功能不足时,线粒体数量增加,平均大小减小。高尔基体仅受到轻微影响。甲状腺功能不足不会改变游离核糖体细胞质聚集体的密度,但内质网密度降低,尼氏体紊乱。