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作者

Wang, JL Xu, FF Zheng, Y Cheng, X Zhang, PP Zhao, HY

作者单位

Shandong Univ, Dept Pediat, Jinan Cent Hosp, Jinan 250013, Shandong, Peoples R China        Shandong First Medical University & Shandong Academy of Medical Sciences     Shandong University Taishan Med Univ, Grad Sch, Tai An 271016, Shandong, Peoples R China        Shandong First Medical University & Shandong Academy of Medical Sciences

刊名

JOURNAL OF INTEGRATIVE NEUROSCIENCE

年份

2019

卷号

Vol.18 No.2

页码

173-179

ISSN

0219-6352

关键词

HIPPOCAMPAL-NEURONS INFLAMMATORY CYTOKINES RAT HIPPOCAMPUS FUNCTIONAL-ROLE PKC-EPSILON INTERLEUKIN-1-BETA EXPRESSION RECEPTOR INVOLVEMENT CURRENTS

摘要

This study aimed to understand the role of Interleukin-1 beta in mouse febrile seizures. To investigate the chronic effects of raised Interleukin-1 beta on seizures, the sodium currents of hippocampal neurons were recorded by whole-cell voltage clamp. Interleukin-1 beta inhibited sodium currents in mouse hippocampal neurons and verified that protein kinase C epsilon contributed to the effect of Interleukin-1 beta exposure. The inhibitory effect was also identified in neurons from a protein kinas...更多

This study aimed to understand the role of Interleukin-1 beta in mouse febrile seizures. To investigate the chronic effects of raised Interleukin-1 beta on seizures, the sodium currents of hippocampal neurons were recorded by whole-cell voltage clamp. Interleukin-1 beta inhibited sodium currents in mouse hippocampal neurons and verified that protein kinase C epsilon contributed to the effect of Interleukin-1 beta exposure. The inhibitory effect was also identified in neurons from a protein kinase C epsilon null mutant mouse. Action potentials were recorded using a ramp depolarizing current. Peak spike depolarization was significantly reduced by Interleukin-1 beta treatment, and was abolished following the administration of a protein kinase C epsilon inhibitor, epsilon V1-2. However, neither Interleukin-1 beta nor epsilon V1-2 had any significant effect on spike threshold. Interleukin-1 beta reduced the amplitude of action potentials due to its inhibitory effect on sodium channels. This is hypothesised to decrease the release of presynaptic transmitters of neuro-excitability, thus exerting a neuroprotective role in excitotoxicity. To ascertain the role of protein kinase C epsilon on febrile seizures in vivo, a heated water-bath model was used to identify susceptible mice. It was found that protein kinase C epsilon reduced susceptibility to, and frequency of, febrile seizure onset. This may be related to the neuroprotective effect of Interleukin-1 beta on hippocampal neurons.收起

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