Abstract

The choroid plexus contains Na K-ATPase-dependent transport systems responsible for the production of the major part of the cerebral spinal fluid (CSF) and the removal of polar metabolites from the ventricular CSF. In adult rabbits, treatment with betamethasone for 5 days decreases choroid plexus Na K-ATPase activity and consequently CSF production and in vitro choroid plexus transport capacity for choline. Choroid plexus Na K-ATPase activity is low in rabbit fetuses. A rapid increase starts at birth and adult levels are reached in around 3 weeks. This increase is parallelled by an increase in the in vitro transport capacity for choline (base) but not for penicillin (acid). Kinetic studies showed no change in Km but an increase in Vmax with age, suggesting that the same carrier system is involved in young and adult animals. Administration of betamethasone to the doe during the last week of pregnancy for 5 days increases fetal choroid plexus Na K-ATPase activity and choline transport capacity by 58-81% and 35% respectively.

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