Muscarinic receptor-mediated increase in cAMP levels in SK-N-SH human neuroblastoma cells

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Abstract

Stimulation of muscarinic cholinergic receptors in SK-N-SH human neuroblastoma cells resulted in a 4–5 fold increase in intracellular cAMP levels. This unusual response was sensitive to atropine and pirenzepine but insensitive to pertussis toxin. It was observable regardless of whether basal, PGE1- or forskolin-stimulated cAMP levels were measured. The half-maximal concentration for carbachol-stimulation of cAMP levels (6 μM) was similar to that for the previously determined carbachol-induced stimulation of phosphoinositide turnover in these cells, suggesting that the former is mediated by the latter. These data indicate that cross-talk between the phosphoinositide turnover system and the adenylate cyclase system results in increased cAMP levels in SK-N-SH cells in response to muscarinic receptor stimulation.

References (15)

  • T. Nabika et al.

    Biochem. Biophys. Res. Comm

    (1985)
  • O.W. Lowry et al.

    J. Biol. Chem

    (1951)
  • V.C. Yu et al.

    J. Biol. Chem

    (1986)
  • D.R. Sibley et al.

    Arch. Biochem. Biophys

    (1986)
  • P.H. Fishman et al.

    Biochem. Biophys. Res. Comm

    (1987)
  • A. Rodriguez-Pena et al.

    Biochem. Biophys. Res. Comm

    (1984)
  • A.G. Gilman

    Ann. Rev. Biochem

    (1987)
There are more references available in the full text version of this article.

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