In carbon monoxide poisoned mice enhanced glycogenolysis and lactate production in the brain are not prevented by pretreatment of the animals with reserpine or an adrenergic β-receptor blocking agent (Kö 592). Since, furthermore, glycogenolysis is not accompanied by changes in the phosphorylase a content or phosphorylase a/phosphorylase (total) ratio, it becomes unlikely that adrenergic mechanisms play a major role in the stimulation of carbohydrate breakdown during carbon monoxide poisoning. It appears more likely that by analogy to the condition in heart glycogenolysis is stimulated by an activation of phosphorylase b due to changes in the concentration of metabolites which are known to inhibit (ATP, glucose-6-phosphate) or activate (AMP, inorganic phosphate) phosphorylase b.