Vasopressin alters female sexual behaviour by acting on the brain independently of alterations in blood pressure

200

Previous studies have provided evidence for a discrete localization of two types of vasopressin (AVP)-labeled binding sites in the rat brain, i.e., regions labeled preferentially with AVP (putative AVP receptors) and regions labeled with AVP as well as oxytocin (OT). The latter binding sites are considered here as putative OT receptors. In the present study the effect of estradiol on the number of these putative receptor sites for OT and AVP was investigated in rat brain after daily subcutaneous administration of the steroid (10 µg/100 g body weight) to ovariectomized rats. Specific binding of [³H]-OT and [³H]-AVP was determined after in vitro incubation of frozen brain sections, autoradiography and quantitation of the images with computer-assisted densitometry. Estradiol increased the number of OT receptors at least 4-fold in the ventromedial nucleus of the hypothalamus, regions of the olfactory tubercle, the nucleus accumbens and occasionally in the organum vasculosum laminae terminalis. A smaller increase (two-fold) was noted in the central amygdala, while a tendency to a decrease in OT receptor number was noted in the olfactory nucleus and the ventral subiculum. Estradiol treatment permitted an estimation of binding constants of [³H]-OT-binding to a membrane fraction of microdissected ventromedial hypothalamic region {K_d: 1.3 nM, B_max: 19.9 fmol/mg protein). The number of putative AVP receptors in the lateral septum and in the nucleus tractus solitarii was not affected by estradiol. In conclusion, the OT receptor system is subject to modulation by estradiol in some discrete brain regions, but not in others. One of the principal sites of this interaction is located in the ventromedial nucleus, which is a hypothalamic region known to contain a high density of estradiol receptors and to respond to estrogens by changes in ultrastructure, protein synthesis, electrophysiology and sexual behavior. The results show that estradiol may sensitize these processes to OT and AVP by increasing the number of putative OT receptors.

mentioning

confidence: 99%

Estradiol Modulates Density of Putative Oxytocin Receptors’ in Discrete Rat Brain Regions

Kloet¹,

Voorhuis²,

Boschma³

et al. 1986

200

“…In other verte brates, AVT and/or arginine vasopressin (AVP) have been shown to influence reproductive behaviors in two species each of mammals [4,14,22] and birds [15], and in one fish species [19].…”

mentioning

confidence: 99%

Autoradiographic Characterization of Binding Sites Labelled with Vasopressin in the Brain of a Urodele Amphibian

Tripp

Moore²

1988

Because arginine vasotocin (AVT) activates male sexual behaviors in the rough-skinned newt (Taricha granulosa), quantitative autoradiography with radiolabelled arginine vasopressin (³H-AVP) was used to characterize putative AVT receptors in the telencephalon of this amphibian. Analyses were restricted to specific binding sites in the medial pallium, although dense binding also was observed in the dorsal pallium and amygdala pars lateralis. Binding of ³H-AVP to these sites was saturable, specific, reversible, of high affinity (Kd= 1 nM) and low capacity (57 fmol/mg protein). The rank order of potency of related peptides in inhibiting ³H-AVP binding was as follows: AVT > d(CH2)5[Tyr(Me)²]AVP (a mammalian pressor antagonist) > AVP, oxytocin, and [dPen¹Tyr(Me)²]AVP (also a pressor antagonist) > mesotocin ≫ desGly(NH2)AVP, AVP fragment 4–9 and pressinoic acid. Thus, these binding sites appear to represent authentic central nervous system receptors for AVT. Furthermore, ligand specificity for the binding sites in this amphibian differ from that reported for AVP binding sites in rat brains. The AVT receptors in the medial pallium, dorsal pallium, and amygdala pars lateralis may represent site(s) of action where AVT elicits sexual behaviors in male T. granulosa.

“…Sodersten et al [26] have demonstrated that vasopressin can terminate heat in OVX rats treated with estradiol and progesterone, and have suggested that a circadian increase in brain vasopressin may play a role in terminating heat in the intact rat. However, if a diurnal increase in vasopressin causes termination of receptivity, it follows that animals should fail to show or show diminished levels of lordosis during the light portion of their light-dark cycle.…”

Section: Discussionmentioning

confidence: 99%

Supplemental Progesterone Delays Heat Termination and the Loss of Progestin Receptors from Hypothalamic Cell Nuclei in Female Guinea Pigs

Brown¹,

Blaustein²

1984

Previous studies indicate that the retention of hypothalamic nuclear progestin receptors parallels the expression of sexual receptivity in ovariectomized, hormonally treated guinea pigs. In this study, the effect of a supplementai progesterone injection on heat termination and retention of nuclear progestin receptors was examined. Ovariectomized guinea pigs were injected with 50 µg progesterone 48 h after receiving 4 µg estradiol benzoate and were tested hourly for lordosis. 8 h after progesterone treatment, animals received either 500 µg progesterone or the oil vehicle. The supplementai progesterone injection delayed the termination of heat by more than 2 h compared to oil-injected animals. The effect of supplemental progesterone on the retention of nuclear progestin receptors was then determined. Animals were killed 8, 10, or 14 h after the initial injection of progesterone, and cytosol and nuclear progestin receptor concentrations in mediobasai hypothalamus-preoptic area were determined. Supplemental progesterone further increased the level of nuclear progestin receptors measured at 10 h, and at 14 h these levels were still elevated above baseline. In contrast, nuclear progestin receptor levels in animals which received only the initial progesterone injection had returned to baseline by 14 h, a time when similarly treated animals were no longer receptive. These results suggest that the mechanism by which heat termination occurs may involve loss of nuclear progestin receptors.