The roles of nicotine on calcium oscillations ([Ca2+]i oscillation) in rat primary cultured cortical neurons were studied. The spontaneous [Ca2+]i oscillations (SCO) were recorded in a portion of the neurons (65%) cultured for 7-10 days in vitro. Application of nicotine enhanced [Ca2+]i oscillation frequency and amplitude, which were reduced by the selective α4β2 nAChRs antagonist DHβE, and the selective α7 nAChRs antagonist MLA (20nM). 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 (20nM) itself reduced SCO frequency without affecting the amplitude, but blocked nicotinic increase in [Ca2+]i oscillation frequency and amplitude. Furthermore, co-administration of both α4β2- and α7- nAChRs antagonists completely prevented nicotinic increment in [Ca2+]i oscillation frequency and amplitude. Thus, our results indicate that both α4β2- and α7- nAChRs mediated nicotine-induced [Ca2+]i oscillations and two nAChR subtypes differentially regulated spontaneous [Ca2+]i oscillation.
- [Ca2+]i oscillations
- α7- nAChRs
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