Epinephrine Effects on Memory Are Not Dependent on Hepatic Glucose Release

Epinephrine released or administered soon after a given training task modulates memory processes. Since epinephrine does not readily cross the blood–brain barrier, studies have suggested that some of the central effects of epinephrine might be mediated by peripheral release of glucose. These experiments examined the involvement of blood glucose levels in the posttraining effects of peripherally administered epinephrine. The effects of the administration of epinephrine (25 and 625 mg/kg) on memory of an inhibitory avoidance task were evaluated in fed and fasted rats (depleted glycogen stores in liver). Blood glucose levels after the task in each group were also measured. Female Wistar rats were divided in two groups. Fed and 48-h-fasted animals were submitted to the inhibitory avoidance task and received ip epinephrine or saline immediately after training. The test session was carried out 48 h after training. Epinephrine (25 or 625 mg/kg) caused an increased glycemia in fed rats, but no effect was observed in fasted animals. Administration of epinephrine 25 mg/kg induced a facilitation of memory, while epinephrine 625 mg/kg impaired retention (either in fasted or in fed animals). There was no relation between increased glycemia induced by epinephrine and its effects on memory, since this drug presented its classical effects independently of the previous state of the animal (fed or fasted). The results of the present study suggest that the effects of systemic released or administered epinephrine on memory processes are not dependent on hepatic glucose release.