SOME EFFECTS OF DIETARY VITAMIN B 6 DEFICIENCY ON γ‐AMINOBUTYRIC ACID METABOLISM IN DEVELOPING RAT BRAIN

— Severe vitamin B 6 deficiency induced in pregnant rats during the last 2 weeks of gestation resulted in a reduction of brain weight in the new born rat. This indicates that the foetus was affected in utero . However, no significant changes were observed in other measured parameters in brains of the neonates at birth. Subjecting these neonates to vitamin B6 deficiency during lactation severely retarded the development of their body and brain weights. There is evidence to suggest that B 6 deficiency also leads to increased levels of glutamic acid decarboxylase apoenzyme, although the in vivo activity of the enzyme appears to be reduced as a result of marked reduction in coenzyme saturation. The level of γ‐aminobutyric acid transaminase apoenzyme was reduced. Its coenzyme saturation was also reduced, but the level of reduction was less than with the decarboxylase. The progressive increase in whole brain γ‐aminobutyric acid level was also retarded by the deficiency. Five days after administration of pyridoxine hydrochloride to 2‐week‐old deficient neonates, whole brain γ‐aminobutyric acid levels and the activities of whole brain glutamic acid decarboxylase and γ‐aminobutyric acid transaminase were almost restored to normal. However, brain and body weight showed a slow recovery during the same period. It was found that in the recovering neonates both enzymes follow changes in age rather than changes in brain weight.