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.