Brain Excitability in Pyridoxine-Deficient Rats

Abstract

The electroshock threshold of rats mildly deficient in pyridoxine rises significantly within 5 hours after the rats are injected with pyridoxine. The electroshock threshold of weight-paired control rats is not affected by the injection of pyridoxine. Cellular hydration reduces the electroshock threshold to a similar extent in normal and pyridoxine-deficient rats. The concentrations of water, sodium, potassium and chloride in the brain and blood plasma and of lactic and pyruvic acid in the blood are the same in pyridoxine-deficient and control rats. Both types of rat have a very mild degree of metabolic acidosis. When extra tryptophane is added to the diet of rats mildly deficient in pyridoxine the signs of deficiency are intensified and there is a fall in electroshock threshold. This fall can be reversed within 5 hours by the injection of pyridoxine. Xanthurenic acid, a product of tryptophane metabolism, when injected into normal rats has no effect on electroshock threshold or maximal seizure pattern. Feeding extra glutamic acid to rats mildly deficient in pyridoxine causes the electroshock threshold to rise. Rats more severely deficient in pyridoxine show a slower rise in electroshock threshold after the injection of pyridoxine, but if the animals have been fed extra glutamic acid for 6 days they respond to injected pyridoxine as rapidly as do mildly deficient rats. It is suggested that the maintenance of normal transaminase activity is essential for those tests of normal brain activity employed in this study.