Glucocorticoid-mediated effects of systemic oxytocin upon memory retrieval.

During the last decade, a considerable amount of evidence has accumulated to show that oxytocin (OT) is involved with functions other than its classical roles in reproduction-associated processes, such as social recognition, maternal behavior and neuroendocrine regulation of the stress response. It has been shown, for instance, that post-training systemic administration of oxytocin in mice produces an amnestic effect on the step-through inhibitory avoidance. Since it is still unclear how systemic levels of OT may affect CNS memory processes, our aim here was to investigate the hypothesis that systemic OT effects on memory retrieval might be mediated through an oxytocin-induced decrease in glucocorticoid release. In our first experiment, we have found an amnestic effect of i.p. pre-test 0.4 microg/kg of OT upon memory retrieval in the inhibitory avoidance task (IA); this OT dose was shown to (a) significantly decrease plasma corticosterone levels when compared to the saline group, and (b) not to cause any anxiety effects by itself in a plus-maze task. At last, an ineffective-by-itself dose of dexamethasone was able to reverse the amnestic effect of this OT dose. Our results suggest that the amnestic effect of systemically administered oxytocin upon memory retrieval in the inhibitory avoidance task was probably caused by an oxytocin-induced decrease in glucocorticoid release from the adrenal gland.