Several Na⁺-dependent carriers of amino acids exist on the abluminal membrane of the blood-brain barrier. These Na⁺-dependent carriers are in a position to transfer amino acids from the extracellular fluid of brain to the endothelial cells and thence to the circulation. To date carriers have been found that may remove non-essential amino acids, nitrogen-rich amino acids, or acidic amino acids (excitatory); all of which may be detrimental to brain function. We describe here Na⁺-dependent transport of large neutral amino acids across the abluminal membrane of the blood-brain barrier that cannot be ascribed to currently known systems. Fresh brains, from cows killed for food, were used. Microvessels were isolated and contaminating fragments of basement membranes, astrocyte fragments and pericytes were removed. Abluminal-enriched membrane fractions from these microvessels were prepared. Transport was Na⁺-dependent, voltage sensitive and inhibited by BCH (2-aminobicyclo(2,2,1)-heptane-2-carboxylic acid), a particular inhibitor of the facilitative LAT1-system. The carrier has a high-affinity for leucine (K_m = 21 µM± 7 SE) and is inhibited by other neutral amino acids including: glutamine, histidine, methionine, phenylalanine, serine, threonine, tryptophan, and tyrosine. Others established neutral amino acids may enter the brain by way of an LAT1-type facilitative transport. The presence of a Na⁺-dependent carrier on the abluminal membrane, capable of removing large neutral amino acids, most of which are essential, from brain, indicates a more complex situation that has implications for the control of essential amino acid content of brain.