Single and multiple courses of antenatal steroids regulate connexin 36 abundance in the ovine fetal brain

Abstract

Connexin 36 (Cx 36) forms gap junctions (GJ). GJ facilitate intercellular communication and are important in neuronal differentiation during development. Cx 36 is the main GJ between neurons, increases during rodent development and is up regulated by dexamethasone (DEX) in pancreatic islets. The effects of steroids on GJ proteins have not been examined in fetal brain. We examined the effects of single and multiple courses of DEX on Cx 36 abundance in the cerebral cortex (CC), cerebellum (CL) and cervical spinal cord (SP), and differences in Cx 36 protein abundance among fetal brain regions. Ovine fetuses at 70% of gestation were examined after a single course of four 6 mg DEX or placebo (PL) injections were given every 12 h for 48 h to the ewes, or the same DEX or PL given course once a wk for 5 wks. Regional brain tissue was frozen after the last DEX or PL dose. Cx 36 protein expression was determined by Western immunoblot. A single course of DEX increased (P < 0.05) Cx 36 protein abundance compared with PL in the CC and SP, and multiple courses increased Cx 36 in SP, but not in CC or CL. Cx 36 was higher in SP than CL. Maternal DEX treatment regulates Cx 36 proteins in vivo in the fetal CC and SP, but not in CL. Different DEX regimens regulate Cx 36 protein abundance in specific brain regions. The greater abundance of Cx 36 protein in SP than CL may suggest the presence of more functional channels in SP in the premature fetal brain.