Introduction. High fructose consumption has been shown to magnify cerebral ischemic injury in the ischemic focus and penumbra region. However, ischemia also produces changes in exofocal areas such as the amygdala, an important structure in emotional processing. Therefore, the objective of the investigation was to characterize the histological changes of the amygdala dendrites caused by high fructose consumption in an experimental model of cerebral ischemia.
Method. Wistar rats fed with standard food were used; the control group was given water and the fructose (HDF) group was given add libitum 20% fructose in water for 11 weeks. Some rats were subjected to cerebral ischemia. Therefore, there were four experimental groups: Sham control, Sham HDF, Ischemia control, Ischemia HDF. 50 um coronal sections of the brains were made and microtubule-associated protein 2 (MAP2) immunohistochemistry was performed. Images were captured and processed in Image J software.
Results. Loss of dendrite immunoreactivity was found in ischemic groups, and also cluster-type MAP2 immunoreactivity in HDF groups.
Conclusion. According to the above, both ischemia and high fructose consumption generate dendritic alterations in the amygdala.
