The Effect of Hypoxia on G Protein Coupled (CB1) Receptor Gene Expression in Cortical B50 Neurons in Culture
View/ Open
Date
2011-02-10Author
Ibegbu, A. O.
Mullaney, I.
Fyfe, Lorna
McBean, Douglas
Metadata
Show full item recordCitation
Ibegbu, A., Mullaney, I., Fyfe, L. & McBean, D. (2011) The Effect of Hypoxia on G Protein Coupled (CB1) Receptor Gene Expression
in Cortical B50 Neurons in Culture, British Journal of Pharmacology and Toxicology, 2(1), pp. 27-36.
Abstract
Hypoxia adversely affects cells and tissues, and neuronal cells in particular have been shown to be
more susceptible to the injurious effects of hypoxia in which they may begin to die when oxygen supply is
reduced or completely eliminated. Cannabinoid (CB1) receptor agonists have been shown to elicit several
Central Nervous System (CNS) effects, mediated via G protein-coupled receptors. The aim of this study was
to examine the effect of hypoxia on G protein coupled receptor (CB1) gene expression in cortical neuronal B50
cell lines in culture. The B50 cells were cultured in normoxia (21% O2; 5% CO2) and hypoxia (5% O2; 5%
CO2), and were treated with cannabinoid agonists to determine their effects on hypoxia-induced changes. Three
cannabinoid agonists [Win55,212-2 mesylate (Win), arachidonoylethanolamide (AEA) and 2-
arachidonylglycerol (2-AG)], were administered to the cells as treatment for 48 hours after 48hours of initial
culture for a total of 96hours of culture in hypoxic conditions at concentrations of 10, 50 and 100 nM. The
levels of G-protein coupled receptor (CB1) mRNAs were assessed using RT-PCR. The results showed that
hypoxia induced morphological changes in B50 cells in hypoxia while the CB1 RT-PCR mRNA levels showed
no appreciable changes in normal, hypoxic and treated cells. The results show that B50 neuronal cells are
susceptible to damage and injurious effects of hypoxia, as are most brain cells and the cannabinoid agonist
treatments showed there were no changes in the level of CB1 receptor gene expression due to hypoxia or agonist
treatment in neuronal B50 cells in culture.