Betamethasone has a specific affinity for type II glucocorticoid receptors which are present in most brain regions. [1]

Betamethasone has direct vasoconstrictor effects on peripheral femoral resistance vessels in late gestation fetal sheep. Betamethasone exposure decreases cerebral blood flow (CBF) in all brain regions measured except the hippocampus after 24 hours of infusion in sheep. [1] Betamethasone reduces the activation of NF-kappaB and elevation of TNFalpha and IL-1beta, and induces the expression of IL-10 in the brain, all of which correlate with the changes of pain thresholds in rats. [2] Betamethasone exposure reduces synaptophysin-LI in the frontal neocortex, caudate putamen and hippocampus by 46.9%, 41.0% and 55.4%, respectively, that is not accompanied by irreversible neuronal damage in the fetal sheep brain. [3] Betamethasone modestly increases cytidylyltransferase (CT) mRNA, but does not alter the levels of immunoreactive enzyme in adult rat lung. Betamethasone decreases the activities of the sphingomyelin hydrolases: acid sphingomyelinase by 33% and of alkaline ceramidase by 21%. [4] Betamethasone injected at the time of nerve injury partially inhibits the development of neuropathic hyperalgesia and reduces the subsequent elevated levels of pro-inflammatory cytokines in the brain of rats, while stimulating the expression of the anti-inflammatory cytokine IL-10. [5]