Patchev V K, Schlosser S F, Hassan A H, Almeida O F
Department of Neuroendocrinology, Max Planck Institute of Psychiatry, Munich, Germany.
Neuroscience. 1993 Dec;57(3):537-43. doi: 10.1016/0306-4522(93)90003-x.
Basal density and estrogen induction of oxytocin binding sites in limbic and hypothalamic structures of the rat brain were investigated by semi-quantitative autoradiography following chronic administration of dexamethasone or progesterone. The selective oxytocin receptor antagonist d(CH2)5[Tyr(Me)2,Thr4,Tyr-NH2(9)] ornithine-vasotocin was used as a ligand for oxytocin binding sites. Estrogen administration increased ligand binding in all sites investigated. Dexamethasone treatment significantly increased ligand binding in the bed nucleus of the stria terminalis, lateral ventral septum and amygdala to an extent which was comparable to that of estradiol alone. In the hypothalamic ventromedial nucleus, dexamethasone significantly decreased basal levels of oxytocin binding. Estrogen administration subsequent to dexamethasone failed to cause a further increase in oxytocin binding in all structures investigated. Chronic progesterone treatment significantly increased basal oxytocin receptor density in the limbic structures, decreased it in the ventromedial nucleus, and prevented estrogen-induced increases in ligand binding in all areas studied with the exception of the medial preoptic area. These findings demonstrate that, in addition to gonadal steroids, glucocorticoids differentially and site-specifically modulate cerebral oxytocin binding sites. The evidence for glucocorticoid and gestagen influences on oxytocin receptors and their inducibility by estrogen may be relevant to the understanding of mechanisms leading to impairment of oxytocin-related behaviours.
