Glycogen is the brain's largest energy store and it is mainly localised in astrocytes. Glycogen turnover is extremely rapid in the brain, especially during sudden increased demand when glucose supplies are insufficient. Previous culture studies have reported on the glycogenolytic effect of noradrenaline on 3--4 week-old primary mouse astrocyte cultures. This effect is believed to be mediated by the beta-adrenergic-cAMP signal transduction system. Recent evidence has shown a drop in forebrain glycogen levels at a specific time point during memory formation for a passive avoidance task in the day-old chick. This 'memory-related' glycogenolysis may be initiated by noradrenaline-induced rises in cAMP occurring around this point, but it is unknown whether astrocytic glycogenolysis is is stimulated by noradrenaline in day-old chicks. This question was approached in the present study and it was shown that noradrenaline is capable of stimulating both cAMP formation and glycogen breakdown in chick primary astrocyte cultures at developmental age (10-14 days in culture) comparable to the newborn chick. In contrast, noradrenaline did not have a corresponding glycogenolytic effect on 10-day-old mouse astrocyte cultures (equivalent to the 1-week mouse), although it induced a considerable amount of glycogen breakdown in older cultures (18 and 24-26 days).