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

Interleukin-1β (IL-1β) 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-1β and NCCs are implicated regulating excitotoxicity and Ca2+ homeostasis, it is not known whether IL-1β modulates NCCs directly. In present study, we examined the effects of IL-1β treatment (10 ng/ml, 24 h) on NCCs in cultured cortical neurons using patch-clamp recording and immunoblot assay. Our results showed that IL-1β decreased NCC currents by ∼50%, which made up 40% of the whole-cell Ca2+ current demonstrated by ω-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-1β. Our finding, IL-1β inhibits the activity of NCC via suppressing NCC protein expression provides new insight into the neuroprotective role of IL-1β in CNS.