Abstract
Interleukin-1β (IL-1β) is a multifunctional proinflammatory cytokine that plays a key role in the injuries and diseases of the central nervous system (CNS). A voltage-gated Na+ channel is essential for the excitability and electrical properties of neurons. However, it is not known whether IL-1β directly affects the central Na+ channels. In the present study, we examined the effects of IL-1β on Na+ currents in cultured cortical neurons using patch-clamp recording. Our results showed that IL-1β suppressed Na+ currents through its receptor in a time- and dose-dependent manner, but did not alter the voltage-dependent activation and inactivation. PKC and then p38 MAPK were involved in this inhibition. The spike amplitude was also inhibited by IL-1β in the doses that decreased the Na+ currents. Our findings revealed the inhibition of chronic IL-1β treatment on voltage-gated Na+ channels in the CNS, and showed that the action potential (AP) amplitude was reduced by IL-1β due to a decrease of Na+ currents.
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Acknowledgments
This work was supported by National Key Basis Research Program of Ministry of Science and Technology of China (973 grant number: 2006CB504105 and 2009CB941301) and National Natural Science Foundation of China (grant number: 30670500 and 30871287).
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Chen Zhou and Cui Qi contributed equally to this work.
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Zhou, C., Qi, C., Zhao, J. et al. Interleukin-1β Inhibits Voltage-Gated Sodium Currents in a Time- and Dose-Dependent Manner in Cortical Neurons. Neurochem Res 36, 1116–1123 (2011). https://doi.org/10.1007/s11064-011-0456-8
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DOI: https://doi.org/10.1007/s11064-011-0456-8