Forskolin-induced Ca
2+ signals were examined in isolated rat olfactory receptor neurons (ORNs) using a Ca
2+ indicator, fura-2. In the soma of the ORNs, forskolin caused an increase in the intracellular Ca
2+ concentration ([Ca
2+]
i) that was enhanced by a phosphodiesterase (PDE) 1 inhibitor, 8-methoxymethyl-3-isobutyl-1-methyl-xanthine, but not a PDE4 inhibitor, rolipram. Forskolin-induced Ca
2+ signals were abolished with the removal of extracellular Ca
2+ and un-affected by treatment with thapsigargin or caffeine plus ryanodine. Niflumic acid, a Ca
2+-activated Cl
− channel inhibitor, or nifedipine, an L-type Ca
2+ channel inhibitor, slowed the initial rate of the increase in [Ca
2+]
i in response to forskolin. Nifedipine did not affect the increase in [Ca
2+]
i that was slowed by niflumic acid. In Ca
2+ measurements with a confocal microscope and a calcium indicator, Fluo-4, the onset of the response to forskolin in the knob region occurred simultaneously or earlier, but not later, than that in the soma. It is suggested that the forskolin-induced Ca
2+ signals are due to Ca
2+ influx, but not the release of Ca
2+ from Ca
2+ stores, and that the initial rapid increase in [Ca
2+]
i is associated with the activation of the voltage-dependent Ca
2+ channels in rat ORNs.
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