Abstract
Although the realization of its special position in brain metabolism inspired clinical glutamic acid therapy, there is as yet no convincing evidence of a connection between the clinical effects and the special metabolic function of glutamic acid in the nervous system. On the other hand there are indications suggesting that the 3 clinical effects which have been described, i.e. the termination of the hypoglycemic coma, the stimulation of intellectual activity in mental deficiency and the alleviation of certain convulsive disorders, are due to an adrenergic mechanism. As far as the effect in hypoglycemic coma is concerned, this view is supported by exptl. evidence. For the other 2 effects it is based on the similarity with the action of sympathomimetic amines. But it should not be overlooked that the adrenergic activity of glutamic acid is probably due to a mechanism different from that underlying the action of sympathomimetic amines, such as amphetamine. Whereas we may assume that glutamic acid stimulates directly the centers of epinephrine production, the effect of sympathomimetic amines is assumed to be due to the inhibition of amine oxidase leading to the prolongation of the life of circulating epinephrine. This difference suggests the combination of the two agents as a rational treatment.