Journal
JOURNAL OF NEUROCHEMISTRY
Volume 74, Issue 4, Pages 1346-1354Publisher
WILEY-BLACKWELL
DOI: 10.1046/j.1471-4159.2000.0741346.x
Keywords
acetylcholine receptor; cyclic AMP; nerve growth factor; nicotinic receptor; PC12 cells; regulation
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To investigate the effects of nerve growth factor (NGF) and cyclic AMP (cAMP) on the revel of the nicotinic acetylcholine receptor subunit alpha 3 mRNA, we used PC12h cells, PC12 cells expressing dominant-negative Ras protein, and the parental PC12 cells, PC12h cells have NGF-responsive tyrosine hydroxylase activity. Expression of dominant-negative Ras protein prevents the signaling through the Ras-mitogen-activated protein kinase cascade. The morphological changes of the parental PC12 cells in response to NGF and 8-(4-chtorophenylthio)adenosine 3',5'-cyclic monophosphate (CPTcAMP), a cell-penetrating cAMP analogue, were similar to those of PC12h cells, NGF up-regulated the alpha 3 mRNA level in PC12h cells and down-regulated the alpha 3 mRNA level in the parental PC12 cells. Expression of dominant-negative Ras protein and an inhibitor of mitogen-activated protein kinase kinase inhibited the effects of NGF on alpha 3 mRNA lever. CPTcAMP down-regulated the alpha 3 mRNA lever in all three PC12 cell lines. An inhibitor of protein kinase A inhibited the CPTcAMP-induced downregulation of alpha 3 mRNA. The alpha 3 mRNA down-regulation required prolonged treatment with CPTcAMP even after cAMP response element binding protein phosphorylation was decreased, Membrane depolarization with high K+ had no effect on the alpha 3 mRNA level in PC12h cells. Based on these results, we propose that at least two unknown effecters regulate alpha 3 mRNA levels in PC12 cells.
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