OXYTOCIN-BINDING SITES IN RAT LIMBIC AND HYPOTHALAMIC STRUCTURES - SITE-SPECIFIC MODULATION BY ADRENAL AND GONADAL-STEROIDS

Basal density and estrogen induction of oxytocin binding sites in limb ic and hypothalamic structures of the rat brain were investigated by s emi-quantitative autoradiography following chronic administration of d examethasone or progesterone. The selective oxytocin receptor antagoni st d(CH2)5[Tyr(Me)2, Thr4, Tyr-NH29] ornithine-vasotocin was used as a ligand for oxytocin binding sites. Estrogen administration increased ligand binding in all sites investigated. Dexamethasone treatment sign ificantly increased ligand binding in the bed nucleus of the stria ter minalis, lateral ventral septum and amygdala to an extent which was co mparable to that of estradiol alone. In the hypothalamic ventromedial nucleus, dexamethasone significantly decreased basal levels of oxytoci n binding. Estrogen administration subsequent to dexamethasone failed to cause a further increase in oxytocin binding in all structures inve stigated. Chronic progesterone treatment significantly increased basal oxytocin receptor density in the limbic structures, decreased it in t he ventromedial nucleus, and prevented estrogen-induced increases in l igand binding in all areas studied with the exception of the medial pr eoptic area. These findings demonstrate that, in addition to gonadal s teroids, glucocorticoids differentially and site-specifically modulate cerebral oxytocin binding sites. The evidence for glucocorticoid and gestagen influences on oxytocin receptors and their inducibility by es trogen may be relevant to the understanding of mechanisms leading to i mpairment of oxytocin-related behaviours.