CD36 Deficiency Suppresses Epileptic Seizures. (26th December 2017)

• Record Type: Journal Article
• Authors: Zheng, Fangshuo; Yang, Yong; Lu, Shanshan; Yang, Qin; Li, Yun; Xu, Xin; Zhang, Yanke; Liu, Feng; Tian, Xin; Wang, Xuefeng
• Is Part Of: Neuroscience. Volume 367(2017)
• Page Start: 110
• Page End: 120
• Publication Date: 2017-12-26
• Subjects: AA arachidonic acid -- ACSF artificial cerebral spinal fluid -- AD Alzheimer's disease -- ANOVA analysis of variance -- APs action potentials -- Aβ amyloid-β peptide -- CD36 cluster of differentiation 36 -- CNS central nervous system -- HEPS (4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid) -- KA kainic acid -- LFPs local field potentials -- LPS lipopolysaccharide -- Mg2+-free ACSF ACSF without MgCl2 -- Nrf2 nuclear factor erythroid-derived 2-like factor 2 -- PD Parkinson's disease -- PPARγ peroxisome proliferator-activated receptor γ -- PTZ pentylenetetrazol -- SE status epilepticus -- SRSs spontaneous recurrent motor seizures -- TLE temporal lobe epilepsy -- TLR toll-like receptor -- WT wild type; CD36 -- epilepsy -- epileptic seizure -- neuronal excitability; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2017.10.024
• Languages: English
• ISSNs: 0306-4522

Abstract

Highlights: The expression of CD36 is increased in epileptic mice. The brain slices from epileptic mice showed that CD36 is co-expressed with neurons in hippocampus. CD36 −/− mice showed an attenuated progression of chronic epilepsy. CD36 deficiency inhibits neuronal firing of APs in the hippocampal slices. CD36 deficiency on LFPs exhibits attenuated massive neuronal electrical activity. Abstract: Cluster of differentiation 36 (CD36) belongs to the class B scavenger receptor family. CD36 is a glycoprotein found on the surface of various cell types and has been implicated in the mechanism of numerous central nervous system (CNS) diseases. However, the relationship between CD36 and epilepsy remains unknown. In this study, we aimed to detect the expression of CD36 in two different chronic epileptic mouse models and determine whether CD36 deficiency leads to suppressive neuronal hyperexcitability and decreased susceptibility of epileptic seizures. Here, we found that CD36 was expressed in the neurons and that CD36 expression was significantly elevated in epileptic mice induced by pentylenetetrazol (PTZ) and kainic acid (KA). Behavioral studies revealed that CD36 deletion in mice (CD36 −/− mice) resulted in an attenuated progression of chronic epilepsy compared with wild-type (WT) mice. Whole-cell patch-clamp technique exhibited a decreased frequency of action potentials (APs) in the hippocampal slices of CD36 −/− mice. In addition, local field potential (LFP) analysis further indicated that CD36 deletion reduced the frequency and duration of epileptiform-like discharges. These results revealed that CD36 deficiency could produce an antiepileptic effect and could provide new insight into antiepileptic treatment.