Long-term nicotine treatment suppresses IL-1β release and attenuates substance P- and 5-HT-evoked Ca²⁺ responses in astrocytes.

The aim of this study was to investigate whether short- or long-term nicotine treatment, had an influence on Ca(2+)-induced intracellular Ca(2+) release in astrocytes co-cultured with microvascular endothelial cells, and if the release of interleukin-1β (IL-1β) changed during this treatment. We found that nicotine-evoked Ca(2+) transients were not attenuated up to 10d of incubation with nicotine, neither was the α7-nicotine acetylcholine receptor (α7-nAChR) protein. After 10d the IL-1β release was decreased. Furthermore, substance P- and 5-hydroxytryptamine (5-HT)-evoked Ca(2+) transients were attenuated after 10d of nicotine treatment, but glial cell line-derived neurotrophic factor (GDNF) had no effect on these transients. The results show that long-term nicotine treatment had no influence on nicotine-evoked Ca(2+) transients or protein expression of the α7-nAChR, but had with a decreased IL-1β release. The Gq protein and inositoltrisphosphate system seems to be influenced by the attenuation of Ca(2+)-evoked intracellular Ca(2+) release after stimulation with substance P and 5-HT.