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

Interleukin-1beta (IL-1beta) 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 Ca(2+) channels (VGCCs), predominantly N-type Ca(2+) channels (NCCs). Although both IL-1beta and NCCs are implicated regulating excitotoxicity and Ca(2+) homeostasis, it is not known whether IL-1beta modulates NCCs directly. In present study, we examined the effects of IL-1beta treatment (10 ng/ml, 24 h) on NCCs in cultured cortical neurons using patch-clamp recording and immunoblot assay. Our results showed that IL-1beta decreased NCC currents by approximately 50%, which made up 40% of the whole-cell Ca(2+) current demonstrated by omega-conotoxin-GVIA, and also significantly downregulated the expression of NCC protein. The residual Ca(2+) currents except L-type Ca(2+) channel currents and NCC currents were not affected by IL-1beta. Our finding, IL-1beta inhibits the activity of NCC via suppressing NCC protein expression provides new insight into the neuroprotective role of IL-1beta in CNS.