Abstract
We have investigated the effects of several neurokine/cytokine family members on the level of α-bungarotoxin-binding to neuronal nicotinic acetylcholine receptors. Exposure of human neuroblastoma cells (SH-SY5Y and IMR-32) to ciliary neurotrophic factor (CNTF), leukemia inhibitory factor or oncostatin-M resulted in a 30–40% decline in α-bungarotoxin receptors on the cells with no decrease seen in either muscarinic acetylcholine receptors or in L-type Ca 2+ channels. The level of nicotinic receptor was not affected by the related cytokine, interleukin-6. Treatment of IMR-32 cells with 40 pM CNTF produced a half-maximal decrease of α-bungarotoxin binding which compared well with the affinity estimated from binding of 125I-CNTF ( K i ≈ 40 pM) and the concentration causing c- fos activation in SH-SY5Y cells, as detected by nuclear run-on assays (60–120 pM). Previous results have indicated that the differentiating agents, phorbol esters and retinoic acid, also decrease nicotinic receptor numbers. Here the effects of CNTF, which did not induce neural differentiation, were enhanced by differentiation with 12- O-tetradecanoylphorbol 13-acetate (10 nM) and prevented by retinoic acid (10 μM). Therefore, the response of neuroblastoma cells to cytokines may be under developmental control. These cells offer a system to examine cytokine responses and signal transduction mechanisms during neural development.
Published Version
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