Abstract
Tashiro (1922) showed that the isolated frog nerve liberates ammonia on stimulation, and Richter and Dawson (1948) have recently found that ammonia is liberated on stimulation by the brain. Ammonia is very toxic to the brain, on which it has an irritant action; but the brain may be protected to some extent by the enzyme system described by Krebs (1935), which can detoxicate ammonia by combination with glutamic acid to form glutamine. Sapirstein (1943) obtained evidence that this system is active in vivo by showing that glutamic acid increases the resistance of animals to convulsions produced by injecting ammonium chloride. The toxic action of ammonia on the brain is also of interest in connection with the view that it may be concerned in certain forms of epilepsy (Harris, 1945). This view is supported by the observations of Price, Waelsch and Putnam (1943) on the inhibitory action of glutamic acid on petit mal attacks.
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