Physiological and drug‐induced changes in the glycogen content of mouse brain

Abstract

1 . The effect of the method of killing on the concentration of glycogen in mouse brain was determined. The cerebral glycogen content of mice killed by immersion in liquid nitrogen did not differ significantly from that of animals decapitated and the heads immediately frozen. A delay before freezing led to the rapid loss of brain glycogen, with a 17% fall at 10 s and an 82% loss after 5 min. 2 . Hyperglycaemia, induced by the administration of d-glucose, resulted in an 8.3% loss of brain glycogen after 120 min. Insulin hypoglycaemia produced a 10.7% fall in glycogen at 60 min followed by an 11.2% increase at 120 min. 3 . Exposure to either high (32° C) or low (10° C) ambient temperatures caused a depletion of brain glycogen. 4 . A circadian rhythm of brain glycogen concentration was found, with a nadir which was coincident with the peak of locomotor activity and body temperature. 5 . Drugs from several pharmacological classes were studied for their in vivo effect on the concentration of glycogen in mouse brain. 6 . Brain glycogen was increased by all the depressant drugs tested, and by some drugs which had little effect on behaviour (diphenhydramine, phenytoin and propranolol), or which caused excitation (caffeine and nialamide). 7 . Glycogen was depleted only by amphetamine-like compounds or by bemegride-induced convulsions. 8 . The results are discussed with particular reference to the possible relation between catecholamines and glycogen metabolism in the brain.