Pollin M M, Griffiths I R
Acta Neuropathol. 1987;73(3):275-80. doi: 10.1007/BF00686622.
A feline dysautonomia of unknown aetiology has been reported in numerous cats in the United Kingdom since 1981. The consistent histological lesion is a chromatolytic-type change within the neurones of the autonomic nervous system, which is also found less frequently in non-autonomic regions, such as the XII nucleus. This study describes the ultrastructural changes in the XII nucleus within the first 2 weeks of clinical disease. In the abnormal neurones there is a dispersion of the Nissl substance, progressing to dilation of individual cisternae by an electron-dense floccular material. Such cisternae have lost the majority of their ribosomes. Normal Golgi complexes can be seen in neurones where there is only slight dispersion of the Nissl substance, but no Golgi complexes, either normal or abnormal, can be identified in any cell in which the Nissl substance is markedly disrupted. There is proliferation of smooth endoplasmic reticulum in several neurones, and there may also be an increased number of morphologically normal mitochondria. The nuclei of affected neurones are eccentric with crenations of the nuclear envelope, and in some cases nucleolar changes are also observed. Autophagic vacuoles are present in small numbers. Other organelles appear normal. These findings compare closely to those for the autonomic neurones, suggesting that the primary effect of the causal agent(s) is on the protein synthetic pathway of specific neurones.
自1981年以来，英国已报告多例病因不明的猫类自主神经功能异常。一致的组织学病变是自主神经系统神经元内的染色质溶解型变化，在非自主区域（如舌下神经核）也较少见。本研究描述了临床疾病前2周内舌下神经核的超微结构变化。在异常神经元中，尼氏体分散，进而被电子致密的絮状物质扩张成单个池。这些池失去了大部分核糖体。在尼氏体仅有轻微分散的神经元中可见正常的高尔基体，但在尼氏体明显破坏的任何细胞中，均未发现正常或异常的高尔基体。几个神经元中有滑面内质网增生，形态正常的线粒体数量也可能增加。受影响神经元的细胞核偏心，核膜有切迹，在某些情况下还观察到核仁变化。自噬泡数量较少。其他细胞器看起来正常。这些发现与自主神经元的发现密切相关，表明致病因子的主要作用是针对特定神经元的蛋白质合成途径。
