Cation permeability of the blood-brain barrier in streptozotocin-diabetic rats

Decreased sodium permeability across the blood-brain barrier occurs in streptozotocin-treated rats after 2 weeks of diabetes. To establish whether this is a phenomenon specific for cations, the blood-brain barrier permeability for sodium, potassium and calcium was studied with an arterial integral uptake technique. Experiments were performed in control rats and, after two weeks after diabetes induction, in untreated streptozotocin-diabetic rats and in insulin-treated streptozotocin rats. In untreated diabetes, the neocortical blood-brain barrier permeability for sodium decreased by 35% (5.2 +/- 1.7 vs 3.4 +/- 1.1 10(-5).cm3.s-1.g-1) and potassium permeability by 39% (19.8 +/- 5.7 vs 12.1 +/- 3.9 10(-5).cm3.s-1.g-1), whereas no differences in calcium permeability occurred. Insulin treatment was associated with an increase in the blood-brain barrier permeability to sodium (4.8 +/- 1.0 10(-5).cm3.s-1.g-1) as compared to untreated diabetes (3.4 +/- 1.1 10(-5).cm3.s-1.g-1). It is concluded that the observed changes in sodium and potassium permeability cannot be caused by electrostatic membrane changes. More specific abnormalities of the transport of sodium and potassium across the blood-brain barrier are likely to occur; disturbances in the sodium-potassium-pump activity could account for such alterations.