Interleukin-1β regulation of N-type Ca2+ channels in cortical neurons

Interleukin-1 beta (IL-1 beta) has been found to play an important role in various diseases in the central nervous system (CNS) and exhibit neuroprotective effects in some conditions. The transmitter release in brain is controlled by voltage-gated Ca2+ channels (VGCCs), predominantly N-type Ca2+ channels (NCCs). Although both IL-1 beta and NCCs are implicated regulating excitotoxicity and Ca2+ homeostasis, it is not known whether IL-1 beta modulates NCCs directly. In present study, we examined the effects of IL-1 beta treatment (10 ng/ml, 24 h) on NCCs in cultured cortical neurons using patch-clamp recording and immunoblot assay. Our results showed that IL-1(3 decreased NCC currents by similar to 50%, which made up 40% of the whole-cell Ca2+ current demonstrated by omega-conotoxin-GVIA, and also significantly downregulated the expression of NCC protein. The residual Ca2+ currents except L-type Ca2+ channel currents and NCC currents were not affected by IL-1 beta. Our finding, IL-1 beta inhibits the activity of NCC via suppressing NCC protein expression provides new insight into the neuroprotective role of IL-1 beta in CNS. (c) 2006 Elsevier Ireland Ltd. All rights reserved.