Examination of topiramat's effects on neuronal apoptosis and astrocyte reactivation after experimentaly induced brain injury with ischemia-reperfusion in rats

Cerebral ischemia is defined as a decrease in cerebral blood flow that causes dysfunction in the brain. The complex interaction of multiple conditions following ischemia, such as inflammation, apoptosis, free radical reactions, together with neuron depolarization, ionic imbalance and the formation of excitotoxic glutamergic signals in the peri-infarction area, results in brain injury. Astrocytes, a type of glial cell, respond to central nervous system damage through a special process called astrogliosis and astrocytes involved in this process are called 'Reactive Astrocytes'. The morphological indicator of reactive astrocytes is the overexpression of GFAP. Topiramate is a new generation anticonvulsant with a broad spectrum mechanism of action. It has a neuroprotective effect because it blocks calcium and sodium channels and reduces glutamate excitotoxicity.These potential mechanisms constitute the pharmacological basis for the treatment of ischemia-reperfusion-induced brain injury. In this study, it is aimed to investigate the effects of topiramate, on neuronal damage leads to apoptosis and reactive changes in astrocytes after experimental ischemia-reperfusion-induced brain injury in rats by immunohistochemical methods; and to statistically evaluate the differences between experimental groups. This examination was performed on the dentate gyrus of the hippocampus. GFAP and Caspase3 staining levels were significantly decreased in the topiramate group compared to the ischemia-reperfusion group. It was thought that topiramate may have a neuroprotective effect on hippocampal neurons and astrocytes in brain injury induced by ischemia-reperfusion.