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Interleukin-6 Regulates Voltage-Gated Sodium channels in a Time- and Dose-Dependent Manner in Rat Cortical Neurons
SHENG Jiangtao 1,GAO fenfei 2,CHEN Weiqiang 3,DENG Lijuan 4,GUO Jingfang 5,WANG Gefei 1,DAI Jianping 1,HUANG Zhengyi 1,SHI Ganggang 2,LI Kangsheng 1 * #
1.Department of Immunology and Microbiology, Shantou University Medical College, Shantou 515041
2.Department of Pharmacology , Shantou University Medical College, Shantou 515041
3.Department of Immunology and Microbiology, Shantou University Medical College, Shantou 515041
4.Department of Endocrinology, Meizhou people's hospital Meizhou, 514031
5.Department of neurosurgery, First affiliated hosptial, Shantou University Medical College, Shantou 515041
*Correspondence author
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Funding: This work is supported by the National Natural Science Foundation of China (No.30972766, 31170852, 81001322, 81172795, 81173048), Specialized Research Fund for the Doctoral Program of Higher Education)
Opened online:17 January 2013
Accepted by: none
Citation: SHENG Jiangtao,GAO fenfei,CHEN Weiqiang.Interleukin-6 Regulates Voltage-Gated Sodium channels in a Time- and Dose-Dependent Manner in Rat Cortical Neurons[OL]. [17 January 2013] http://en.paper.edu.cn/en_releasepaper/content/4513574
 
 
The cytokine interleukin-6 (IL-6) is expressed at elevated levels within the CNS in many neurological disorders and may contribute to the histopathological, pathophysiological, and cognitive deficits associated with such disorders. However, the effects of chronic IL-6 exposure on neuronal function in the CNS are largely unknown. A voltage-gated Na+ channel is essential for the excitability and electrical properties of neurons. Therefore, using patch-clamp recording we investigated the effects of chronic IL-6 exposure on voltage-gated Na+ channels. Our results showed that IL-6 suppressed Na+ currents through its receptor in a time- and dose-dependent manner, but did not alter the voltage-dependent activation and inactivation. The spike amplitude was also inhibited by IL-6 in the doses that decreased Na+ currents. The present data reveals chronic exposure to elevated levels of IL-6, such as occurs in various neurological diseases, produces inhibition in the voltage-gated Na+ channels without the alterations in single-channel characteristics. The results support the hypothesis that chronic IL-6 exposure can disrupt normal CNS function and thereby contribute to the pathophysiology associated with many neurological diseases.
Keywords:interleukin-6; Voltage-Gated Sodium channels; Cortical Neurons; patch-clamp recording
 
 
 

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