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Nongenomic Mechanisms of Glucocorticoid Inhibition of Nicotine-Induced Calcium Influx in PC12 Cells: Involvement of Protein Kinase C¹

Neuroscience Research Institute, Second Military Medical University (J.Q., S.-J.L., Y.-z.C.); and the Key Laboratory of Neurobiology, Shanghai Institute of Physiology (J.Q.), the Shanghai Institute of Cell Biology (L.-g.L., G.P.), and the Beijing Institute of Developmental Biology (X.-y.H.), Chinese Academy of Sciences, Shanghai 200433, China

Address all correspondence and requests for reprints to: Dr. Y. Z. Chen, Neuroscience Research Institute, Second Military Medical University, 800 Xiang Yin Road, Shanghai 200433, 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 Gö6976. 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⁺ influx induced by Nic through the pertussis toxin-sensitive G protein-PKC pathway and that PKC plays an important role in the mechanisms of glucocorticoid nongenomic action.

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