Feline dysautonomia: an ultrastructural study of neurones in the XII nucleus.

Abstract

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.