Electron microscopic research of the optic nerve in an experiment with toxic neuritis

Abstract

Рurpose. To identify ultrastructural changes of the optic nerve in the area of the trellis plate in rabbits after exposure to methyl alcohol. Material and methods. A model of experimental optic neuritis with the introduction of methyl alcohol into the retrobulbar space was reproduced on 8 rabbits. The animals were removed from the experiment on the 14th, 30th, 90th and 180th days after the administration of methanol. Pieces of the optic nerve (1–2 mm) were isolated from the enucleated eyeballs in the area of the lattice plate and examined using a transmission electron microscope. Results. On the 14th day after the administration of methanol, signs of pronounced cytoplasmic edema and destruction of intracellular organelles were detected in the ganglion neurons of the rabbit retina in the area of the lattice plate. In individual nerve fibers of the optic nerve, myelin sheaths were stratified and unfolded, axons swelled. Structural changes were detected in astrocytes, especially in the processes around blood vessels. Macrophages of nervous tissue — microgliocytes — became active. Morphological changes indicated a violation of microcirculation and permeability of the hematoneural barrier. The basal membranes around the walls of blood vessels were compacted. Intracellular organelles were destroyed in the cytoplasm of endothelial cells, hemostasis was determined inside the vessels. Subsequently, on the 30–90th day of the experiment, dystrophic and destructive changes in the cytoplasm of ganglion cells and their processes forming the optic nerve, as well as surrounding gliocytes progressed. There were signs of gliofibrosis. Destructive processes and gliofibrosis of the retina and nerve fibers of the optic nerve in the area of the lattice plate increased in degree of expression up to 180th days of the experiment. Conclusion. The results of electron microscopic studies of the intrabulbar part of the optic nerve in experimental animals in dynamics after the introduction of methyl alcohol indicate that the main trigger for the development of visual neuritis may be a violation of microcirculation processes in the retina and optic nerve, which leads to an increase in the permeability of the hematoneural barrier. These events entail dystrophic and destructive changes in the nervous tissue, the progression of which naturally leads, with the assistance of glial cells to gliofibrosis of the optic nerve. Keywords: toxic optic neuritis, methanol, hematoneural barrier, axon demyelination, gliofibrosis