The roles of nicotine on Ca(2+) oscillations [intracellular Ca(2+) ([Ca(2+)]i) oscillation] in rat primary cultured cortical neurons were studied. The spontaneous [Ca(2+)]i oscillations (SCO) were recorded in a portion of the neurons (65%) cultured for 7-10 days in vitro. Application of nicotine enhanced [Ca(2+)]i oscillation frequency and amplitude, which were reduced by the selective α4β2-nicotinic acetylcholine receptors (nAChRs) antagonist dihydro-β-erythroidine (DHβE) hydrobromide, and the selective α7-nAChRs antagonist methyllycaconitine citrate (MLA, 20 nM). DHβE reduced SCO frequency and prevented the nicotinic increase in the frequency. DHβE somewhat enhanced SCO amplitude and prevented nicotinic increase in the amplitude. MLA (20 nM) itself reduced SCO frequency without affecting the amplitude but blocked nicotinic increase in [Ca(2+)]i oscillation frequency and amplitude. Furthermore, coadministration of both α4β2- and α7-nAChRs antagonists completely prevented nicotinic increment in [Ca(2+)]i oscillation frequency and amplitude. Thus, our results indicate that both α4β2- and α7-nAChRs mediated nicotine-induced [Ca(2+)]i oscillations, and two nAChR subtypes differentially regulated SCO.
Keywords: calcium; intracellular calcium ion concentration oscillations; nicotine; α4β2-nicotinic acetylcholine receptors; α7-nicotinic acetylcholine receptors.
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