Abstract
The blood-brain barrier functionally resides in the cerebral vascular endothelium which creates a dynamic regulatory interface between the blood and brain tissue front. As has been long recognized, the cerebral vascular endothelium, unlike endothelial cells found in other vascular beds, lacks numerous fenestrae and vesicles and further adjacent endothelial cells are joined by tight junctions creating a continuous endothelial membranous interface between the blood and brain tissue. As would be anticipated, this continuous endothelial sheet permits the passage of only those solutes that are lipid soluble, of low molecular weight and not highly ionized. Nutrients, on the other hand, which are polar compounds cannot easily cross through such a continuous membrane. This potential problem, however, has been obviated by tlie existence of multiple carrier systems that allow for the facilitated diffusion of the various nutrients from blood to brain front. To date, seven carrier-mediated systems have been identified allowing for the passage of glucose, monocarboxylic acids, neutral amino acids, basic amino acids, purine bases, amines and nucleosides (Pardridge, 1985). These carriers are believed to exist on both the luminal and abluminal endothelial membranes, allowing for effective flux of nutrients from blood to brain and brain to blood. In addition to these facilitated transport mechanisms, active transport has also been demonstrated in relation to the blood-brain barrier. However, in this case, this energy requiring process is believed confined to the abluminal endothelial surface. Here it is envisioned that active transport functions to remove potassium against a concentration gradient from the brain microenvironment to the blood front. Similarly, it has also been speculated that damaging excitatory amino acids such as glutamate are selectively sequestered and moved from the brain to blood front via such active transport mechanisms (Pardridge, 1979).