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Delbro, D., Westerlund, A., Bjorklund, U. and Hansson, E. (2009) In inflammatory reactive astrocytes co-cultured with brain endothelial cells nicotine-evoked Ca2+ transients are attenuated due to interleukin-1a release rearrangement of actin filaments. Neuroscience, 159, 770-779.
http://dx.doi.org/10.1016/j.neuroscience.2009.01.005?

has been cited by the following article:

• TITLE: Nicotine induces intracellular Ca2+ increases in cultured hippocampal astrocytes by nAChR-dependent and -independent pathways

  AUTHORS: Miriam Hernández-Morales, Jesús García-Colunga

  KEYWORDS: Glial Cells; Hippocampus; Nicotinic Acetylcholine Receptors; Potassium Channels; Calcium Signaling; Astrocytes

  JOURNAL NAME: World Journal of Neuroscience, Vol.4 No.1, January 20, 2014

  ABSTRACT: Nicotine, the major addictive substance in tobacco, interacts with nicotinic acetylcholine receptors (nAChRs) located in neuronal and glial cells, modulating synaptic transmission and memory. Here, we show that nAChRs agonists, including nicotine, acetylcholine, and choline, increase the intracellular Ca2+ concentration ([Ca2+]i) in cultured hippocampal astrocytes, indicating the involvement of nAChRs. Interestingly, inhibition of nAChRs, with a cocktail of antagonists (mecamylamine, methyllycaconitine plus dihydro-β- erythroidine), does not prevent the astrocytic [Ca2+]i increases generated by nicotine. This last effect would be attributable to inhibition of K+ currents by nicotine in these cells, as previously we showed using patch- clamp recordings. Furthermore, the application of tetraethylammonium, an inhibitor of K+ currents, also increases the [Ca2+]i. Together, these results indicate that nicotine increases [Ca2+]i in hippocampal astrocytes through two pathways: by activation of nAChRs, and likely by direct inhibition of K+ currents.