Growth Factor‐Like Effects Mediated by Muscarinic Receptors in PC12M1 Cells

Ronit Pinkas‐Kramarski, Reuven Stein, Liora Lindenboim, Mordechai Sokolovsky*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Abstract: Rat pheocromocytoma (PC12) cells stably expressing cloned m1 muscarinic acetylcholine receptors (PC12M1) undergo morphologic changes when stimulated by muscarinic agonists. These changes, which include the outgrowth of neurite‐like processes, are blocked by the muscarinic antagonist atropine and are not observed in PC12 cells. The observed morphological changes, which are independent of RNA and protein synthesis, are blocked by the methylation inhibitor 5′‐deoxy‐5′‐methylthioadenosine, suggesting that methylation plays a role in this process. Analysis of cyclic AMP accumulation and phosphoinositide turnover reveals that both processes are enhanced on activation by muscarinic agonist. Our data suggest, however, that the muscarinic‐dependent neurite‐like outgrowth processes are not mediated by cyclic AMP, Ca2+, or protein kinase C pathways. The muscarinic‐dependent neurite outgrowth effect is enhanced by nerve growth factor, with a resulting increase in both the number of neurite‐extending cells and the length of the neurite. In addition, activation of muscarinic receptors in PC12M1 cells stimulates the induction of marker genes for neuronal differentiation. Muscarinic receptors may therefore mediate growth factor‐like effects in these cells.

Original languageEnglish
Pages (from-to)2158-2166
Number of pages9
JournalJournal of Neurochemistry
Issue number6
StatePublished - Dec 1992


  • Differentiation
  • Gene induction
  • Muscarinic receptor
  • Neuritic outgrowth
  • PC12


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