Investigating the Remyelination Effects of Myricetin After Demyelination Caused by Experimental Pressure Applied to the Optic Chiasm in Rats

Background/Objectives The aim of this study was to induce demyelination in rats by placing a balloon catheter applying pressure under the optic chiasm using a stereotaxic device, and subsequently examine the effects of myricetin, a neuroprotective agent, on the demyelination/remyelination processes using electron microscopy. Methods A total of 40 adult male Wistar albino rats were used to establish an experimental model of optic chiasm compression via stereotaxic placement of a neuroballoon catheter. Animals were divided into four groups: control, demyelination, remyelination, and myricetin treatment. After catheter-induced compression, demyelination and remyelination processes were evaluated. Myricetin was administered intraperitoneally in the treatment group. Optic chiasm tissues were harvested and analyzed histopathological and ultrastructurally using electron and light microscopy. Statistical analyses were performed using chi-square tests, with p< 0.05 considered significant. Results When the demyelination and remyelination groups were compared with the control group, severe degeneration accompanied by Wallerian degeneration was observed, along with demyelination in axons, vacuolization in oligodendrocytes, and dark axonal degeneration. Compared to the other groups, the myricetin group showed a reduction in dark degeneration, axonal demyelination, and degeneration. Conclusions This study represents another example of experimental models of demyelination resulting from optic chiasm compression, which are rare in the literature. Myricetin has been shown to have positive effects on remyelination and may guide subsequent studies. Furthermore, this experimental model may allow the investigation of the demyelination and remyelination effects of different agents in the optic chiasm.