Respiratory surveillance and inward rectifier potassium channel expression in lung tissue within an experimental epilepsy model

Abstract

Epilepsy is characterized by neuronal discharges that occur as a result of disruption of the excitatory and inhibitory balance of the brain due to functional and structural changes. It has been shown in the literature that this neurological disorder may be related to the expression of ion channels. Any defect in the function or expression mechanism of these channels can lead to various neuronal disorders such as epilepsy. Epileptic seizures occur as a result of the accumulation of biological disorders in the circulatory, respiratory and nervous systems. In this study, we aimed to examine the changes in the expression of inward-directing potassium channels (Kir 3.1 and 6.2) in lung tissue and respiratory functions, considering that it will contribute to the elucidation of the mechanisms of sudden deaths thought to be caused by cardiorespiratory complications in epilepsy. In the study, 48 adult male Wistar albino rats weighing 250–300 g were used in the study. During the research process, respiratory function tests were performed on epileptic rats induced with pentylenetetrazol (PTZ) firing model, and then histopathological changes in lung and hippocampus tissues, and expression levels of the Kir (3.1 and 6.2) channels were evaluated by immunohistochemistry, qRT-PCR and Western blot analysis. Memantine and tertiapin-Q have been shown to protect epileptic groups from histopathological harm induced by PTZ application and also reduce HIF-1α, Kir 3.1 and Kir 6.2 expression. The findings imply that memantine and tertiapin-Q would be suitable options for treating epilepsy patients.