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Gap junctions are specialized membrane structures that mediate intercellular communication and facilitate passage of ions and small molecules between adjacent cells. Connexins comprise a multigene family of transmembrane proteins that form gap junctions. Connexin-32 and connexin-43 are among the most abundant connexins in brain and are highly expressed during development. Connexin-32 is expressed primarily in oligodendrocytes and connexin-43 in astrocytes in adult brain. However, both connexins are expressed in neurons during development. We examined the effects of ontogeny on connexin-32 and connexin-43 protein abundance in cerebral cortices of sheep during development. Western immunoblot was used to measure connexin-32 and connexin-43 expression in cerebral cortices of fetuses at 60%, 80%, and 90% of gestation, in newborn lambs and adult sheep. Values were expressed as ratios to a single adult control cerebral cortical sample. Connexin-32 abundance was higher (P

Maternal treatment with corticosteroids reduces blood-brain barrier permeability in premature ovine fetuses and the incidence of intraventricular hemorrhage in premature infants. We tested the hypothesis that maternally administered corticosteroids increase the expression of tight junction (TJ) proteins in the cerebral cortex of ovine fetuses with and without exposure to in-utero brain ischemia. Fetuses at 80% of gestation were studied 18 h after the last of four 4−6 mg dexamethasone or placebo injections were given over 48 h to ewes. Groups were placebo/control, dexamethasone/control, placebo/ischemic, and dexamethasone/ischemic. Ischemia consisted of 30 min of fetal carotid artery occlusion and 72 h of reperfusion. Cerebral cortex was snap frozen. Western immunoblot was used to measure the protein expression of occludin, claudin-1, claudin-5, zonula occludens (ZO)-1, and ZO-2, and a TJ accessory protein annexin II. Occludin and annexin II protein expression were 48% and 58% higher (P