Nongenomic Mechanisms of Glucocorticoid Inhibition of Nicotine-Induced Calcium Influx in PC12 Cells: Involvement of Protein Kinase C* * This work was supported by a research grant from the Natural Science Foundation of China.

Nongenomic mechanisms of corticosterone (B) inhibition of nicotine (Nic)-induced calcium influx were investigated in PC12 cells. Corticosterone could rapidly inhibit the Ca2+ influx induced by Nic, and BSA-conjugated B had a similar inhibitory effect. The inhibition of Nic-induced Ca2+ influx by B could be mimicked by protein kinase C (PKC) activator (phorbol 12-myristate 13-acetate) and reversed by PKC inhibitors, chelerythrine chloride and Go6976. When PC12 cells were pretreated with pertussis toxin, the inhibitory effect of B on Nic-induced Ca2+ influx was blocked. Both B and BSA-conjugated B could activate PKC activity, with the maximal responses at 10−9 and 10−7 m at 37 C, respectively. The dose-response curve was bell shaped. At 25 C, however, the dose-response curve considerably shifted to the right, and B was most potent at 10−5 m. The time course showed that PKC activity was highest at 5 min of B’s action. The results suggest that B might act via putative membrane receptors and inhibit the Ca2+ i...

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