Dexamethasone attenuates inflammatory-mediated suppression of β2-adrenoceptor expression in rat primary mixed glia

Abstract β2-adrenoceptors are G-protein coupled receptors expressed on both astrocytes and microglia that play a key role in mediating the anti-inflammatory actions of noradrenaline in the CNS. Here the effect of an inflammatory stimulus (LPS + IFN-γ) was examined on glial β2-adrenoceptor expression and function. Exposure of glia to LPS + IFN-γ decreased β2-adrenoceptor mRNA and agonist-stimulated production of the intracellular second messenger cAMP. Pre-treatment with the synthetic glucocorticoid and potent anti-inflammatory agent dexamethasone prevented the LPS + IFN-γ-induced suppression of β2-adrenoceptor mRNA expression. These results raise the possibility that inflammation-mediated β2-adrenoceptor downregulation in glia may dampen the innate anti-inflammatory properties of noradrenaline in the CNS.