The mechanism of mitochondrial autophagy regulating CME in epilepsy

Abstract

Mitophagy is a process of removing damaged mitochondria, transferring damaged mitochondria to lysosomes for degradation, thereby regulating the quality of mitochondria and maintaining the stability of the intracellular environment. CME(Clathrin-mediated-endocytosis)plays an important role in the endocytosis and recovery of vesicles. It is also the main way for large parts of substances to enter cells, and it is widely involved in the signal transduction of various physiological activities of cells. Therefore, this study used pentylenetetrazol to ignite the abnormal mitochondrial autophagy in the chronic epilepsy model and the epilepsy model without magnesium-induced neurons. Subsequently, the autophagy inhibitor 3-MA was used to further observe that the inhibition of autophagy caused a decrease in the fluorescence uptake of Tf-A488 in the primary cultured neurons and the hippocampus of experimental mice, and the inhibition of mitochondrial autophagy could inhibit the function of CME. Finally, through PTZ epilepsy model and kainic acid model, we observed the effect of 3-MA on epilepsy behavior and its in-body field potential, and finally clarify the possible mechanism of mitochondrial autophagy regulating CME and participating in epilepsy.