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Molecular basis of limbic epilepsy

Molecular basis of limbic epilepsy

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中国神经科学学会第十届全国学术会议

作者： Zhi-Qi Xiong Institute of Neuroscience the Chinese Academy of Sciences

epilepsy is a common and refractory neurological disorder,but the neuronal regulatory mechanisms of epileptogenesis remain largely ***-dependent transcription of neurotrophins such as brain-derived neurotrophic factor（BDNF） has been shown to promote epileptogenesis;however,little is known about factors that may act as intrinsic,homeostatic or counter-balancing *** we show that limbic seizure activity up-regulated NRGl/ErbB4 signaling,and that epileptogenesis was inhibited by intracerebral infusion of NRGl,but exacerbated by neutralizing endogenous NRGl with soluble ecto-ErbB4,by inhibiting ErbB4,or by deleting the ***,specific depletion of ErbB4 in parvalbumin（PV）-expressing interneurons abolished NRGl-mediated inhibition of epileptogenesis and promoted kindling progression,resulting in increased spontaneous seizures and exuberant mossy fiber *** contrast,depleting ErbB4 in CaMKIIα-positive pyramidal neurons had no ***,NRG1-induced activation of ErbB4 in PV-expressing inhibitory intemeurons may serve as a critical endogenous negative-feedback mechanism to suppress limbic epileptogenesis.

关键词： limbic epilepsy ErbB4 parvalbumin CaMKⅡα

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Neuregulinl represses limbic epileptogenesis via activation of ErbB4 signaling in parvalbumin-positive interneurons

Neuregulinl represses limbic epileptogenesis via activation ...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Guo-He TAN~(1,★),Yuan-Yuan LIU~(1,★),Xiao-Ling HU~1,Dong-Min YIN~2,Lin MEI~(2,*),Zhi-Qi XIONG~(1,*) 1 Institute of Neuroscience and State Key Laboratory of Neuroscience,Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences,Shanghai 200031,China 2 Program of Developmental Neurobiology and Department of Neurology,Institute of Molecular Medicine and Genetics,Georgia’s Health Sciences University,Augusta,GA 30912,USA

Objective epilepsy is a common and refractory neurological disorder that affects l%-2%worldwide people,but the neuronal regulatory mechanisms of epileptogenesis remain largely ***-dependent expression of polypeptide growth factors has been implicated in epileptogenesis;however,little is known about factors that may act as intrinsic,homeostatic or counter-balancing *** this study,we investigated the role of a growth factor neuregulin 1(NRG1) and its ErbB4 receptor in limbic *** Two classical models of limbic epilepsy,kindling and pilocarpine models,were used to investigate the expression pattern of NRG1 and ErbB4. Using lose- and gain- of- function strategies,we determined the role of NRG1/ErbB4 signaling in epileptogenesis pharmacologically and ***/loxP-mediated cell-specific mutation was employed to identify the specific cellular mechanism underlying the effect of this signaling in limbic ***(1) limbic seizure activity increased the expression of Nrg1 and phosphorylation of ErbB4 receptor in the brain.(2) In kindling model, epileptogenesis was inhibited by intracerebral infusion of recombinant NRG1,but exacerbated by neutralizing endogenous NRG1 with soluble ecto-ErbB4.(3) Pharmacologically,inhibition of ErbB4 activity with PD158780 greatly promoted kindling-induced epileptogenesis.(4) Genetically,heart-rescued ErbB4 knockout mice exhibited accelerated progression of the kindling effect.(5) Specific depletion of ErbB4 in parvalbumin(PV)-positive GABAergic interneurons resulted in accelerated kindling ***,NRG1 infusion failed to suppress kindling development in PV-Cre;ErbB4 mice.(6) Deletion of ErbB4 in CaMKIIα-positive pyramidal neurons was ineffective for epileptogenesis,as evidenced by normal kindling progression of both CaMKIIα-iCre;ErbB4 and CaMKIIα-CreER;ErbB4 mice.(7) Ablation of ErbB4 in PV-positive neurons increased kindling-induced brain hyperexcitability and spo

关键词： limbic epilepsy epileptogenesis neuregulin 1 ErbB4 parvalbumin-positive interneurons

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