Choline enters brain by saturable transport at the blood–brain barrier (BBB). In separate studies, both sodium-dependent and passive choline transport systems of differing affinity have been reported at brain capillary endothelial cells. In the present study, we re-examined brain choline uptake using the in situ rat brain perfusion technique. Saturable brain choline uptake from perfusion fluid was best described by a model with a single transporter (Vmax= 2.4–3.1 nmol/min/g; Km = 39–42 µm) with an apparent affinity (1/Km) for choline five to ten-fold greater than previously reported in vivo, but less than neuronal ‘high-affinity’ brain choline transport (Km = 1–5 µm). BBB choline uptake from a sodium-free perfusion fluid using sucrose for osmotic balance was 50% greater than in the presence of sodium suggesting that sodium is not required for transport. Hemicholinium-3 inhibited brain choline uptake with a Ki (57 ± 11 µm) greater than that at the neuronal choline system. In summary, BBB choline transport occurs with greater affinity than previously reported, but does not match the properties of the neuronal choline transporter. The Vmax of this system is appreciable and may provide a mechanism for delivering cationic drugs to brain.