Anandamide-induced neuroblastoma cell rounding via the CBI cannabinoid receptors

Isao Ishii, Jerold Chun

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

The CBI cannabinoid receptor has been shown to couple with pertussis toxin (PTX)-sensitive Gi/o proteins and inhibit adenylyl cyclase. However, in certain conditions, CBI mediates adenylyl cyclase activation, possibly through Gs-type G proteins. In rat BI03 neuroblastoma cells in which CBI gene was endogenously expressed, anandamide inhibited forskolin-induced cAMP accumulation via PTX-sensitive pathways. When CBI 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 CBI-over-expressing BI03 cells, anandamide induced cell rounding via a PTX-insensitive/Rho kinase inhibitor-sensitive pathway. These results suggest that the CBI receptor could couple with G proteins that activate Rho (possibly G12/13) as well as Gi/o and Gs.

Original languageEnglish
Pages (from-to)593-596
Number of pages4
JournalNeuroReport
Volume13
Issue number5
Publication statusPublished - 2002 Apr 16
Externally publishedYes

Fingerprint

Cannabinoid Receptors
Pertussis Toxin
Neuroblastoma
Colforsin
Adenylyl Cyclases
rho-Associated Kinases
rho GTP-Binding Proteins
GTP-Binding Proteins
anandamide
Genes
Proteins

Keywords

  • Adenylyl cyclase
  • Anandamide
  • Cannabinoid
  • CBI
  • Cell rounding
  • G protein
  • Neuroblastoma
  • Pertussis toxin
  • Receptor
  • Retrovirus

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Anandamide-induced neuroblastoma cell rounding via the CBI cannabinoid receptors. / Ishii, Isao; Chun, Jerold.

In: NeuroReport, Vol. 13, No. 5, 16.04.2002, p. 593-596.

Research output: Contribution to journalArticle

Ishii, Isao ; Chun, Jerold. / Anandamide-induced neuroblastoma cell rounding via the CBI cannabinoid receptors. In: NeuroReport. 2002 ; Vol. 13, No. 5. pp. 593-596.
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