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Ethanol Exposure Potentiates fos B and jun B Expression Induced by Muscarinic Receptor Stimulation in Neuroblastoma SH‐SY5Y Cells
Author(s) -
Ding WeiQun,
Fried Ulrik,
Larsson Christer,
Ailing Christer
Publication year - 1998
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1998.tb03642.x
Subject(s) - muscarinic acetylcholine receptor , carbachol , protein kinase c , stimulation , endocrinology , chemistry , sh sy5y , medicine , microbiology and biotechnology , biology , receptor , kinase , neuroblastoma , cell culture , biochemistry , genetics
Muscarinic receptor stimulation and activation of protein kinase C cause an increase in fos B and jun B transcripts in human neuroblastoma SH‐SY5Y cells. In this study, the effect of long‐term ethanol exposure on these events was investigated. Carbachol‐stimulated fos B and jun B expression was elevated in ethanol‐exposed cells compared with control cells. The potentiation was time‐ and dose‐dependent on ethanol. Preincubation with muscarinic antagonists or protein kinase C inhibitor demonstrated that the carbachol‐stimulated increase in fos B and jun B mRNA levels was primarily mediated via M1 receptors and dependent on the activity of protein kinase C in both control and ethanol‐exposed cells. Long‐term ethanol exposure did not influence the expression of fos B and jun B induced by activation of protein kinase C with phorbol ester. These results demonstrate that the muscarinic receptor‐stimulated fos B and jun B expression is sensitive to ethanol exposure in SH‐SY5Y cells, suggesting that these genes participate in the regulation of neuronal function in response to chronic ethanol treatment.