Vk. Patchev et al., OXYTOCIN-BINDING SITES IN RAT LIMBIC AND HYPOTHALAMIC STRUCTURES - SITE-SPECIFIC MODULATION BY ADRENAL AND GONADAL-STEROIDS, Neuroscience, 57(3), 1993, pp. 537-543
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.