Nongenomic mechanisms of glucocorticoid inhibition of nicotine-induced calcium influx in PC12 cells: Involvement of protein kinase C

Jian Qiu, Li Guang Lou, Xiu Ying Huang, Shu Jie Lou, Gang Pei, Yi Zhang Chen

Research output: Contribution to journalArticle

61 Scopus citations

Abstract

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 PC 12 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.

Original languageEnglish (US)
Pages (from-to)5103-5108
Number of pages6
JournalEndocrinology
Volume139
Issue number12
DOIs
StatePublished - Jan 1 1998

ASJC Scopus subject areas

  • Endocrinology

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