The Effect Of CD36 Deletion Involved In Epilepsy

Epilepsy is a common,chronic,neurological disease characterized by recurrent seizures.The abnormal electrical activity generated by massive neuronal hypersynchrony is supposed to underlie the critical pathology of epilepsy.Cluster of differentiation 36（CD36）is a membrane glycoprotein belonging to the class B scavenger receptors and has broad ligand specificity.By binding to different ligands,CD36 has been implicated in multiple biological processes,including metabolism of fatty acid,engulfment and removal of endogenous metabolites and production of inflammatory mediators.Recently,several studies have shown that CD36 is involved to play a critical role in the pathophysiology of a number of central nervous system diseases.However,the relationship between CD36 and epilepsy remains unknown.This study aimed to investigate the expression pattern of CD36 in two different chronic epileptic mouse models,and to determine if CD36 deletion can affect epileptic seizures and change the excitability of hippocampal neuron.Western bloting was used to detect the expression of CD36 and found that its expression was both significantly elevated in epileptic mice induced by pentylenetetrazol（PTZ）and kainic acid（KA）.Behavioral study revealed that CD36 gene knockout(CD36^-/-)mice showed delayed latency and decreased severity of epileptic seizures in two chronic epilepsy models compared to wild-type（WT）mice.Whole-cell patch-clamp technique exhibited decreased frequency of action potentials（APs）in the hippocampal slices of CD36 knockout mice.Moreover,the result of local field potentials（LFPs）records further demonstrated that CD36 deletion decreased the frequency and duration of epileptiform-like discharges in the hippocampal CA1 region.These results revealed that epileptic activity could increase the expression levels of CD36 protein,and CD36 deletion could take an anti-epileptic effect.It could provided a new insight into a potential pharmacologic target in epilepsy treatment.