Department of Physiology, University of Utah School of Medicine, Salt Lake City
1. The electroshock threshold of rats mildly deficient in pyridoxinerises significantly within 5 hours after the rats are injectedwith pyridoxine.
2. The electroshock threshold of weight-pairedcontrol ratsis not affected by the injection of pyridoxine.
3. Cellular hydration reduces the electroshock threshold toa similar extent in normal and pyridoxine-deficient rats.
4.The concentrations of water, sodium, potassium and chloridein the brain and blood plasma and of lactic and pyruvic acidin the blood are the same in pyridoxine-deficient and controlrats. Both types of rat have a very mild degree of metabolicacidosis.
5. When extra tryptophane is added to the diet ofrats mildlydeficient in pyridoxine the signs of deficiencyare intensifiedand there is a fall in electroshock threshold.This fall canbe reversed within 5 hours by the injection ofpyridoxine.
6. Xanthurenic acid, a product of tryptophanemetabolism, wheninjected into normal rats has no effect onelectroshock thresholdor maximal seizure pattern.
7. Feedingextra glutamic acid to rats mildly deficient in pyridoxinecausesthe electroshock threshold to rise.
8. Rats more severelydeficient in pyridoxine show a slowerrise in electroshock thresholdafter the injection of pyridoxine,but if the animals have beenfed extra glutamic acid for 6 daysthey respond to injectedpyridoxine as rapidly as do mildlydeficient rats.
9. It issuggested that the maintenance of normal transaminaseactivityis essential for those tests of normal brain activityemployedin this study.
1 This work was supported by United States Public Health ServiceResearch Grant 155-c for the Study of the Physiology and Therapyof Convulsive Disorders.