Hong Ni
Soochow University, China
Title: Autophagy and zinc / lipid metabolism mediated plasma membrane integrity signaling participates in the pathophysiological process of epileptogenesis
Biography
Biography: Hong Ni
Abstract
Developmental seizures are one of the most common clinical emergencies in pediatric neurology and a significant proportion of children evolve into epilepsy in adulthood. The mechanism of epileptogenesis has not been elucidated yet. Our research has tentatively revealed the possible mechanism from the following aspects: First, autophagy signaling pathway involved in the acute neuronal excitotoxic injury and cell loss in forebrain, as well as long-term neurobehavioral injury and pathological changes of the hippocampus, Intraperitoneal injection of autophagy inhibitors(3- MA, CBI, E-64d) immediately after seizures inhibited these long-term adverse consequences. Second, regenerative sprouting of mossy fibers in the hippocampus is one of the causes of epileptogenesis and is thought to be a pathological basis for the hyperexcitability of brain neurons. Our study found that there were abnormal expressions of zinc ion transporters and lipid metabolism molecules in the long-term hippocampus and was highly correlated with each other, which was in parallel with the sprouting. Long-term application of metabolic regulation methods, such as ketogenic diet, leptin, and melatonin , can inhibit the sprouting and neurobehavioral injury. Finally, our preliminary study suggests that autophagy and zinc / lipid metabolism signaling pathways interact and participate in the pathophysiological process of epileptogenesis, which might be a new target for repair of neuronal plasma membrane damage following developmental seizures.