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. 2008 Dec 16;3(12):e3945. doi: 10.1371/journal.pone.0003945

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Kawakita et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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Nicotine-stimulated calcium signaling was investigated by the use of a fluorescent Ca²⁺ indicator. Primary chondrocyte cultures were stimulated by nicotine with or without MLA, the specific antagonist of alpha7 homomeric nAChR. A: Addition of assay buffer alone elicits no reaction (upper panels: negative control). Nicotine elicits a transient increase of intra-cellular calcium (lower panels). B: Nicotine elicits a transient increase of intra-cellular calcium in a concentration-dependent manner. C: MLA inhibits nicotine-induced calcium influx in a concentration-dependent manner. The cells were treated with MLA 30 min before nicotine stimulation.