The brain of a rat in which uremia has been experimentally induced does not demonstrate the changes of edema. The uremic brain is more permeable as measured with inert molecules such as sucrose and inulin. The increased permeability of uremic brain would permit more ready entry into brain of dialyzable toxic compounds present in uremic sera. There is a slowing of sodium entry and increase in potassium entry, suggesting alterations in membrane ion pump activities. The brain is less permeable to penicillin in uremia, probably reflecting the accumulation of organic acids in this disorder which competitively inhibit a membrane transport system. The role of this organic acid transport system in normal brain metabolism is not known. Elucidation of these derangements of membrane function in uremic brain may explain the diverse neurological manifestations of uremic encephalopathy.