IGF-1 regulates cAMP levels in astrocytes through a β2-adrenergic receptor-dependant mechanism

Abstract

We have recently demonstrated that neonatal astrocytes derived from mice lacking beta-2 adrenergic receptors (beta(2)AR) possess higher proliferation rates, as compared to wild-type cells, an attribute that was shown to involve insulin-like growth factor (IGF) signaling. In the present study, we demonstrate that basal cAMP levels in beta(2)AR knockout astrocytes were significantly lower than in wild type cells. Furthermore, treatment with IGF-1 reduced intracellular cAMP levels in wild type astrocytes, yet had no effects on cAMP levels in beta(2)AR deficient astrocytes. Our data suggests that IGF-1 treatment influences cAMP production through a beta(2)AR-dependant mechanism in astrocytes. A deficit of beta(2)AR on astrocytes, as previously reported in multiple sclerosis, may influence cell proliferation, an action which could have implications in processes involved in astrogliosis.