Inhibition of cyclic AMP formation in N1E-115 neuroblastoma cells is mediated by a non-cardiac M2 muscarinic receptor subtype

Wanida Surichamorn, Carla L. Amrhein, Carlos Forray, Esam E. El-Fakahany

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

The cardioselective muscarinic antagonist, AF-DX 116 ((11[2-[(diethyl-amino)-methyl]-O-1-piperidinyl]-5,11-dihydro-6H-pyrido-[2,3-b][1,4]-benzodiazepine-6-one), was weak at blocking the M2 muscarinic receptor-mediated inhibition of cyclic adenosine monophosphate (cAMP) formation in mouse neuroblastoma cells (clone N1E-115). In contrast, the glandular-selective antagonists, hexahydro-sila-difenidol (HHSiD) and 4-diphenylacetoxy-N-methyl-pipedinine methiodide (4-DAMP), were quite potent at inhbiting this response, being 14- and 318-fold more potent than AF-DX 116 in this regard, respectively. According to the rank order of potency of these two classes of antagonists, these data provide the first pharmacological evidence that inhibition of cAMP formation in a neuronal tissue is mediated by a non-cardiac M2 muscarinic receptor subtype.

Original languageEnglish (US)
Pages (from-to)320-325
Number of pages6
JournalBrain Research
Volume493
Issue number2
DOIs
StatePublished - Jul 31 1989

Bibliographical note

Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.

Keywords

  • 4-Diphenlacetoxy-n-methyl-piperidine methiodide
  • AF-DX 116
  • Hexahydro-sila-difenidol, Cyclic adenosine monophosphate
  • Muscarinic receptor subtypes
  • N1E-115 neuroblastoma

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