Memory-enhancing effect of posttraining epinephrine is not blocked by dexamethasone

Abstract

There is extensive evidence that stress-related honnones administered shortly before or after training on a variety oftasks can influence retention (de Wied, 1984;McGaugh, 1983). Such evidence suggests that hormones released by learning experiences may serve as endogenous modulators of memory storage (Gold & McGaugh, 1984).Recently, Tilders, Berkenbosch, Vermes, Linton, & Smelik (1985) reported that a number of honnones, in addition to corticotrophin releasing factor (CRF) , induce the release of adrenocorticotropic honnone (ACTH) from the pituitary cortex in vitro. The hormones found to release ACTH include epinephrine, norepinephrine, arginine vasopressin, oxytocin, angiotensin 11, vasoactive intestine polypeptide (VIP), and histidine isoleucinamide. Since several of these honnones have been found to influence memory, these findings suggest that a common action by which the honnones affect memory storage might involve the release of ACTH from the anterior pituitary.Many studies have shown that posttraining administration of epinephrine alters retention: Low doses generally enhance retention, whereas high doses impair retention (McGaugh, 1983; McGaugh & Gold, in press). Epinephrine is known to stimulate the release of ACTH in vivo (Berkenbosch, Vennes, Binnekade, & Tilders, 1981;Reisine, Heisler, Hook, & Axelrod, 1983; Tilders, Berkenbosch, & Smelik, 1982) as weH as in vitro. Epinephrine is released from the adrenal medulla and is a ligand for both Q(-and ß-receptors in the periphery. Available evidence indicates that epinephrine crosses the blood-brain baITier poorly, if at a1l (Weil-Malharbe, Axelrod, & Tomchick, 1959). The effects of epinephrine on retention are blocked by a variety of Q(-and ß-adrenoreceptor antagonists (Sternberg, Korol, Novack, & McGaugh, 1986). Considered together, such findings suggest that epinephrine may influence memory storage through effects initiated at peripheral receptors.In the present study we sought to determine whether the effect of epinephrine on memory storage is mediated

Role of ACTH in recovery from retrograde amnesia induced by hypothermia in rats.

“…Although these data clearly indicate that ACTH is important in mediating recovery from experimentally induced amnesia, a recent report suggests that this hormone may not be as critical with respect to memory enhancement. McGaugh et al (1987) have reported that epinephrine-induced memory enhancement in rats was not related to a congruency of ACTH at training and testing. This finding suggests that drug-induced memory enhancement may be different from recovery from amnesia and, as such, may be mediated by different psychobiological processes.…”

“…Data from control groups discounted alternative interpretations focusing on stress-induced performance artifacts. For example, dexamethasone administration before training or testing did not interfere with the animal's ability to learn or to perform the passive avoidance task, respectively–a conclusion previously made by other investigators (e.g., Beatty et at., 1970; Kasper-Pandi et at., 1970; McGaugh, Bennett, Liang, Juler, & Tam, 1987). Although plasma measures of ACTH after dexamethasone treatment were not available, indirect evidence of dexa-methasone's effect is seen in reduced body weights.…”