Epilepsy is the most common neurological disease in clinical pediatrics. In the past 20 years, more than 10 new antiepileptic drugs (AEDs) have been put into the clinical line and have achieved significant efficacy in controlling symptoms, but they fail to provide therapeutic benefit in 20-25% of patients. To make matters worse, these AEDs often result in serious physiological and psychological harm to patients. Thus, looking for compounds that prevent the epileptogenesis is expected to provide new approaches for the treatment of developmental seizure induced brain damage.
The term epileptogenesis refers to the transformation of the normal neuronal network into a long lasting chronically hyperexcitable state. Strong evidence exists that pathological change such as aberrant mossy fiber spouting in hippocampus due to developmental seizure can irreversibly alter synapse formation through activity-dependent mechanisms, leading to susceptibility to seizures in the adult brain that may result in neurofunctional impairment.
Hippocampal mossy fibers (MFs) are the axons of dentate gyrus granule cells, which could generate aberrant regenerative sprouting (a pathological hallmarks associated with mesial temporal lobe epilepsy) when overstimulated in both clinical symptomatic temporal lobe seizures and epileptic animals.
Numerous hypotheses have been advanced to explain the deleterious changes of axon spouting, including excitatory/inhibitory receptor pathway, direct action of zinc transporters and altered lipid metabolism, reflected in part by activation of phospholipases, neutral sphingomyelinase, as well as newly founded plasticity related genes (PRGs). However, the exact mechanisms are still unclear. This Research Topic will focus on revealing the molecular signals of MFs sprouting so as to provide new therapeutic target for inhibiting epileptogenesis. The Topic Editors welcome contributions in the form of original research papers, technical reports and reviews.
Epilepsy is the most common neurological disease in clinical pediatrics. In the past 20 years, more than 10 new antiepileptic drugs (AEDs) have been put into the clinical line and have achieved significant efficacy in controlling symptoms, but they fail to provide therapeutic benefit in 20-25% of patients. To make matters worse, these AEDs often result in serious physiological and psychological harm to patients. Thus, looking for compounds that prevent the epileptogenesis is expected to provide new approaches for the treatment of developmental seizure induced brain damage.
The term epileptogenesis refers to the transformation of the normal neuronal network into a long lasting chronically hyperexcitable state. Strong evidence exists that pathological change such as aberrant mossy fiber spouting in hippocampus due to developmental seizure can irreversibly alter synapse formation through activity-dependent mechanisms, leading to susceptibility to seizures in the adult brain that may result in neurofunctional impairment.
Hippocampal mossy fibers (MFs) are the axons of dentate gyrus granule cells, which could generate aberrant regenerative sprouting (a pathological hallmarks associated with mesial temporal lobe epilepsy) when overstimulated in both clinical symptomatic temporal lobe seizures and epileptic animals.
Numerous hypotheses have been advanced to explain the deleterious changes of axon spouting, including excitatory/inhibitory receptor pathway, direct action of zinc transporters and altered lipid metabolism, reflected in part by activation of phospholipases, neutral sphingomyelinase, as well as newly founded plasticity related genes (PRGs). However, the exact mechanisms are still unclear. This Research Topic will focus on revealing the molecular signals of MFs sprouting so as to provide new therapeutic target for inhibiting epileptogenesis. The Topic Editors welcome contributions in the form of original research papers, technical reports and reviews.