The loss of consciousness in hypoglycaemia is generally regarded as a direct consequence of the fact that the brain cells are being increasingly deprived of glucose, their principal fuel. The prompt relief of symptoms by glucose administration led to a number of investigations on the effect of other substrates known to sustain the respiration of surviving brain slices in vitro. Amongst these are various mono- and disaccharides, and such acids as lactic, pyruvic, succinic or glutamic acid which may be formed from glucose in the course of its metabolism. It appeared, however, that, in contrast to their in vitro action, most of these substances, including glutamic acid, were unable to relieve the symptoms of hypoglycaemia in eviscerated or hepatectomized animals (Bollmann and Mann, 1931; Maddock, Hawkins and Holmes, 1939). Similarly, lactic and pyruvic acids were found to have no effect on the oxygen consumption of the brain or the comatose state of hypoglycaemic patients undergoing insulin shock therapy (Wortis and Goldfarb, 1940; Goldfarb and Wort is, 1941). It has been shown for several substrates, including glutamic acid, that their rate of diffusion from the blood stream into brain tissue was markedly slower than that of glucose, and that therefore the concentration necessary for the maintenance of nervous function was not reached (Klein, Hurwitz and Olsen, 1946; Klein and Olsen, 1947). In harmony with this are the observations of Fried berg and Greenberg (1947), and of Waelsch, Schwerin and Bessman (1949) that intravenously injected glutamic acid is not taken up by brain tissue. The differences between the in vitro and in vivo results seemed to be adequately explained by these experiments.