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Anandamide-induced neuroblastoma cell rounding via the CB1 cannabinoid receptors

Academic Article
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Overview

authors

  • Ishii, I.
  • Chun, Jerold

publication date

  • April 2002

journal

  • Neuroreport  Journal

abstract

  • The CB1 cannabinoid receptor has been shown to couple with pertussis toxin (PTX)-sensitive Gi/o proteins and inhibit adenylyl cyclase. However, in certain conditions, CB1 mediates adenylyl cyclase activation, possibly through Gs-type G proteins. In rat B103 neuroblastoma cells in which CBI gene was endogenously expressed, anandamide inhibited forskolin-induced cAMP accumulation via PTX-sensitive pathways. When CB1 was heterologously over-expressed using a retroviral transfer, high concentrations of anandamide increased forskolin-induced cAMP accumulation, and this effect was more prominent when cells were pretreated with PTX. In CB1-over-expressing B103 cells, anandamide induced cell rounding via a PTX-insensitive/Rho kinase inhibitor-sensitive pathway. These results suggest that the CB1 receptor could couple with G proteins that activate Rho (possibly G12/13) as well as Gi/o and Gs.

subject areas

  • Animals
  • Arachidonic Acids
  • Calcium Channel Blockers
  • Cannabinoids
  • Cell Size
  • Cyclic AMP
  • Dose-Response Relationship, Drug
  • Endocannabinoids
  • Mice
  • Mice, Inbred C57BL
  • Neuroblastoma
  • Polyunsaturated Alkamides
  • Rats
  • Receptors, Cannabinoid
  • Receptors, Drug
  • Tumor Cells, Cultured
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Research

keywords

  • CBI
  • G protein
  • adenylyl cyclase
  • anandamide
  • cannabinoid
  • cell rounding
  • neuroblastoma
  • pertussis toxin
  • receptor
  • retrovirus
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Identity

International Standard Serial Number (ISSN)

  • 0959-4965

Digital Object Identifier (DOI)

  • 10.1097/00001756-200204160-00011

PubMed ID

  • 11973452
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Additional Document Info

start page

  • 593

end page

  • 596

volume

  • 13

issue

  • 5

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