Evidence for involvement of midbrain central gray in cholinergic mediation of female sexual receptivity in rats.

Conducted 3 experiments with 63 female Sherman rats to determine the role of the midbrain central gray (MCG) in facilitation of lordosis by cholinergic agonists. Selected findings show that Ss with MCG damage displayed significantly less facilitation than sham-lesion Ss. Pretreatment with scopolamine (SCOP) abolished lordosis facilitation in both groups, and after treatment with estradiol and progesterone, sham-lesion Ss showed more receptivity than MCG-lesion Ss. Systemic injection of SCOP produced a significant decline in lordosis for both groups. Results suggest that the MCG plays an important role in the cholinergic mediation of female sexual receptivity. (21 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Aggressive behavior in female hamsters: The hormonal basis for fluctuations in female aggressiveness correlated with estrous state.

The frequency and sequencing of aggressive behaviors by naive female hamsters has been found to change during series of brief encounters, probably because of the lack of stable dominance relations. Such initial encounters seem most representative of interactions likely in free-ranging hamsters and have been emphasized in studies of the hormonal mediation of female aggression. The present 4 experiments, conducted with a total of 72 random-bred female hamsters, found that nonestrous females exhibited intense aggression toward conspecifics of either sex. Estrous females were not aggressive and spent much time in lordosis, indicative of sexual receptivity. While oil-injected adrenalectomized-ovariectomized females fought at high levels, comparable with intact nonestrous females, the combination of 17-β-estradiol benzoate and progesterone suppressed fighting completely. In contrast, replacement of estradiol, progesterone, or testosterone propionate individually had no consistent effect. Hypophysectomized females also fought at high levels, indicating that pituitary hormones are not required for vigorous aggression. Further, individual anterior pituitary hormones did not produce marked changes in fighting. Results emphasize the roles of estrogen and progesterone in synchronizing aggression with current reproductive state. (36 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of repeated testing on sexual behavior of the female rat.

Investigated effects of stimulation during repeated testing, using 24 female Sprague-Dawley rats in which intromission was prevented by a vaginal mask. Ss were ovariectomized and administered 1 mg of estradiol benzoate (EB) daily for 10 days (Exp I) or 5 mg of EB for 2 days (Exp II). Behavioral indices included lordosis quotient (a measure of sexual receptivity) and rejection quotient (a measure of social rejection of the male). Intensity and duration of lordosis gave additional measures. In Exp I hourly testing increased lordosis quotient and duration, especially in Ss receiving EB for 5 days; no effects of daily testing were shown. Exp II compared the behavior of Ss that were either handled hourly and tested hourly with the male rat or only handled hourly to the behavior of Ss that were tested and handled only once. Repeated testing and/or handling facilitated sexual responsiveness, while Ss that received neither treatment were sluggish in their social response to the male rat when they were tested, and were not sexually receptive. (17 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Hypophysectomy facilitates sexual behavior in female rats

Lordosis was elecited in 49% of 87 hormonally untreated, hypophysectomized-ovariectomized (hypox-ovx) female rats in response to palpation of the flanks and perineum (vaginal stimulation was not applied). By contrast, only 12% of 113 hormonally untreated ovariectomized (ovx) rats showed lordosis in response to such stimulation. Subsequently, hypox-ovx and ovx-only rats were given daily injections of 1 mug/kg estradiol benzoate (EB) and tested for sexual receptivity with males. Teh estrogen-treated hypox-ovx females became sexually receptive significantly earlier, and exhibited higher lordosis quotients and more soliciting behavior, than the estrogen-treated ovx-only rats. The increased sexual responsiveness in the hypox-ovx rats could be due to increased LRH activity. To test this, we treated hypox-ovx rats with dihydrotestosterone propionate (DHT-P), which suppresses plasma LH levels but is relatively ineffective in inducing sexual receptivity, and found a significant depression of lordosis responsiveness. These experiments suggest that hypox-ovx females show a heightened responsiveness to hormonal and/or sensory factors that induce a lordosis response, possibly because of increased LRH activity.     

Concurrent inhibition of sexual behavior, but not brain [–3H]estradiol uptake, by progesterone in female rats.

In 7 experiments with ovariectomized female Sprague-Dawley rats, chronic injections of high doses of progesterone (5 mg) and low doses of estradiol benzoate (EB; 2 μg) resulted in less sexual behavior than did low doses of progesterone (.5 mg) and low doses of EB. In a typical procedure for inducing sexual behavior, EB and progesterone were given sequentially, separated by 42 hrs. High levels of progesterone (2.5 and 5 mg) administered concurrently with EB inhibited the induction of sexual receptivity. Increasing the dose of EB from 2 μg to 6 μg or 10 μg offset this inhibition. High doses inhibited the induction of sexual behavior, but the inhibition waned when progesterone was administered 48 hrs prior to EB. A single injection of progesterone (1 mg) that did not inhibit the induction of sexual behavior when administered concurrently with EB did inhibit lordosis when distributed into 5 injections (.2 mg) every 4 hrs. Results of 2 experiments in which progesterone did not inhibit the uptake or retention of [–3H]estradiol by brain cell nuclei suggest that the antiestrogenic action of progesterone in the CNS is not to interfere with the binding of estradiol. (37 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Evidence that a factor besides progesterone, prolactin, or plasma-estradiol-binding protein inhibits estrogen-induced sexual receptivity in pregnant rats.

Reexamined in 4 experiments the assumption that progesterone is responsible for the inhibition of estrogen-induced receptive behavior in Wistar hooded rats. Daily administration of estradiol benzoate (EB) stimulated significantly less lordotic behavior during the 2nd half of pregnancy than in ovariectomized Ss that received sc progesterone implants, pituitary grafts that raised plasma prolactin, or both treatments combined. Following an initial facilitation of receptivity, Ss with progesterone implants showed only moderate reductions in lordosis quotients over 3 test days. The capacity of Ss' plasma to bind estradiol was found to increase significantly during the 2nd half of pregnancy. However, daily administration of a synthetic estrogen, R 2858, which is not bound by plasma protein, was no more effective than EB in stimulating receptive behavior. Administration of EB also stimulated significantly lower levels of sexual behavior in pregnant Ss than in Ss in which pseudopregnancy had been prolonged by previous hysterectomy or induction of uterine decidualization. These findings suggest that some endocrine factor other than progesterone, prolactin, or estradiol-binding protein is primarily responsible for the potent suppression of behavioral responsiveness to estrogen that occurs in pregnant rats. It is suggested that 5-alpha-reduced androgens may cause these behavioral effects. (53 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Binding of [3H]estradiol by brain cell nuclei and female rat sexual behavior: inhibition by experimental diabetes

In streptozotocin-diabetic female rats acute (24 h) withdrawal of insulin significantly impairs both estradiol + progesterone-induced sexual receptivity and cell nuclear concentration of [3H]estradiol in hypothalamus, preoptic area, and pituitary gland. Omission of insulin treatment for the first 24 h of a 30-h or 54-h estradiol benzoate-conditioning period significantly reduced mean lordosis ratings of ovariectomized-diabetic rats. Insulin withdrawal at the time of progesterone treatment and behavioral testing did not diminish sexual receptivity. One-half or 2 h after an intravenous injection of [3H]estradiol-17beta diabetic rats without insulin exhibited reduced cell nuclear [3H]estradiol concentrations (2 h) and/or diminished cell nuclear/whole homogenate concentration ratios (0.5 and 2 h). Twenty-four hour insulin withdrawal affected neither whole tissue [3H]estradiol uptake nor hypothalamus-preoptic area cytoplasmic estrogen-receptor content. These results: (1) suggest that diminished estradiol binding by target tissue cell nuclei may contribute to the well-known reproductive failures of female diabetics, and (2) support the concept that estradiol acts at the level of brain cell nuclei to induce female sexual behavior.     

Somatosensory determinants of lordosis in female rats: Behavioral definition of the estrogen effect.

By coating the ventral surface of 16 Sprague-Dawley male rats with a dye, regions of contact between males and females ( n = 76) during male mounting were recorded precisely on the female's hair and skin. Film analyses showed that the male's paws and pelvic thrusting stimulated the female's skin with dominant frequencies between 10 and 20/sec. Somatosensory stimuli were then applied to the female skin locations contacted by the male. Deflection of hair on the flanks or perineum alone did not cause lordosis. Light stimulation simultaneously on flanks and perineum caused lordosis only in some females given high estrogen dosages supplemented by progesterone. When flank stimuli were followed by pressure on the rump, tailbase, and perineum, lordosis was triggered reliably in hormone-treated females. In this case, the estrogen-dependence of the reflex was shown, and progesterone synergized with the estrogen effect. Among lordosis components, rump and head elevations in response to pressure stimuli on the rump, tailbase, and perineum appear to be hormone-sensitive. (20 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Forebrain sites of estradiol-17!b action on sexual behavior and aggression in female Syrian hamsters.

The effects of intracranial implants of estradiol in the ventromedial hypothalamus (VMH), the anterior hypothalamus (AH), or the medial amygdala (AMG) on aggression, sexual behavior, and serum estradiol were examined in female Syrian hamsters. Estradiol implants in the VMH, followed by systemic progesterone, stimulated sexual behavior and inhibited aggression. Estradiol implants in other intracranial sites activated sexual behavior but did not reliably inhibit aggression. Intracranially implanted and systemically treated animals had equivalent peripheral estradiol concentrations at sacrifice. Results suggest that (1) the VMH is an important neural site for estradiol actions on sexual and aggressive behavior, (2) the caudal AH and AMG may also be sites of estradiol action on sexual behavior, and (3) intracranial implants may only be effective given systemic estradiol exposure or the concurrent stimulation of multiple brain areas. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Estradiol induces hypothalamic progesterone receptors but does not activate mating behavior in male hamsters (Mesocricetus auratus) before puberty.

This study investigated pubertal changes in neural and behavioral responses to estradiol. Gonadectomized pre- and postpubertal male hamsters (Mesochcetus auratus) were treated with 0.00, 0.05, 0. 10, or 0.2 mg estradiol and tested 1 week later for sexual behavior with a receptive female. Estradiol activated behavior in postpubertal, but not prepubertal, males. In contrast, estrogen receptor α (ERα) and progesterone receptor (PR) immunoreactivity in forebrain nuclei that mediate mating behavior was similar in pre- and postpubertal males. Thus, absence of a behavioral response before puberty is not associated with reduced levels of steroid receptors. Because estradiol induced PR in prepubertal males these data also suggest that ERα is functional before puberty. Therefore, gonadal steroids facilitate male reproductive behavior only after as-yet-unidentified developmental processes occur during puberty. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Medial preoptic area oxytocin and female sexual receptivity.

Intracerebroventricular (icv) administration of the nonapeptide oxytocin (OXT) increases sexual receptivity in female rats. The medial preoptic area (MPOA) appeared to be the most sensitive brain area to the facilitative effects of OXT. Bilateral infusions of 100 ng of OXT into the MPOA significantly elevated lordosis quotients in overiectomized (OVX), estrogen-treated rats. This dose of OXT was ineffective when infused icv or into the ventromedial hypothalamus, mesencephalic central gray, or ventral tegmental area. A 500-ng dose of OXT significantly elevated lordosis responding when infused icv, corresponding with our previous findings. Mounting by males significantly increased immunoreactive levels of OXT and decreased the number of OXT immunostaining cells in the MPOA of sexually receptive rats pretreated with estrogen and progesterone. The MPOA is a primary site of the OXT facilitation of sexual receptivity where OXT may be released during mating. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Cholinergic influences on estrogen-dependent sexual behavior in female rats.

Examined the ability of cholinergic agents to influence hormone-dependent sexual behavior in Sherman rats. In Exp I, sexual behavior, indicated by the incidence of lordosis, was significantly increased in estrogen-treated Ss following bilateral infusion of a cholinergic receptor agonist, carbachol (.5 μg/cannula) into the medial preoptic area of the brain. Infusion of an artificial cerebrospinal fluid vehicle failed to facilitate lordosis. The incidence of lordosis was normally highest 15 min after carbachol infusion began to wane by 45 min, and had returned to control levels by 90 min. Centrally administered carbachol activated lordosis at lower levels of estrogen priming than did systemically administered progesterone. In Exp II, Ss brought into sexual receptivity by administration of estrogen and progesterone received preoptic infusions of an acetylcholine synthesis inhibitor, hemicholinium-3 (HC-3). Significant reductions in the incidence of lordosis were observed following bilateral infusion of HC-3 (1.25 μg/cannula). This inhibition of lordosis was prevented when carbachol (.5 μg/cannula) was infused along with HC-3. Results confirm the importance of cholinergic influences on sexual behavior in female rats. (20 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Unconditioned sexual incentive motivation in the male Norway Rat (Rattus norvegicus).

Sexual incentive motivation was evaluated in a procedure consisting of a large open field where incentive animals were confined behind wire mesh openings. When sexually inexperienced male rats (Rattus norvegicus) were exposed to the receptive female-male incentives, they spent more time close to the female. If the incentives were receptive female-nonreceptive female, the receptive female was preferred. However, when the alternatives were nonreceptive female-male, no preference was obtained. Castration abolished preference for the receptive female, and treatment with testosterone propionate restored it. Estradiol plus oil is as efficient as estradiol plus progesterone for giving the ovariectomized female incentive properties. The living female can be replaced with female odor. Sexual experience did not have any long-term effects on the female's incentive value, but immediately preceding limited sexual activity enhanced it. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Mesencephalic participation in the control of sexual behavior in the female rat.

In 2 experiments with 78 female albino rats, electric stimuli applied to both pudendal nerves evoked field potentials, unit responses, and multiunit responses in the ventrolateral midbrain, in and around the peripeduncular nucleus. Bilateral lesions placed in this region suppressed sexual behavioral responses (lordosis and courting behavior) of ovariectomized Ss primed with 5, 10, 100, and 1,000 μg of estradiol benzoate and 2 mg/kg progesterone. It is proposed that the region in question represents a relay station for the integration of sensory and endocrine information concerned in the control of receptive sexual behavior in the female rat. (54 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Role of pelvic nerves in the postcopulatory abbreviation of behavioral estrus in female rats

The role of the pelvic nerves in the postmating abbreviation of behavioral estrus in domestic female rats was investigated. Mating during a period of 40 min at the beginning of hormonally induced estrus in spayed female rats resulted in a rapid decrease in receptivity as measured hourly by the lordosis response. Moreover, the length of the receptive period was significantly shortened by mating at the start of the period. Bilateral pelvic nerve transection completely abolished these effects of mating. Continuous exposure to sexually active males throughout the period of receptivity resulted in a more pronounced decline in receptivity but again was without effect in pelvectomized females. Apparently genital stimuli mediated by the pelvic nerves are responsible for the postcopulatory decrease in receptive behavior in the female rat.     

Vaginal stimulation in rats induces prolonged lordosis responsiveness and sexual receptivity.

Conducted 2 experiments, using a total of 131 female Sprague-Dawley rats. Sexual receptivity to males resulted from stimulation of the vagina with a glass rod in previously unreceptive ovariectomized, estrogen-treated Ss. Several minutes of rejection behavior preceded the receptivity. In Exp II manual palpation was used to determine the duration of the lordosis response facilitation. Initially, all Ss were unresponsive to manual flank-perineum stimulation (palpation). Vaginal stimulation plus palpation, which together elicited lordosis, facilitated subsequent lordosis responses to palpation. This effect persisted for several hours after the vaginal stimulation was applied. Vaginal stimulation alone, which was ineffective in eliciting lordosis, also facilitated lordosis in response to subsequent palpation. Repeated palpation did not facilitate lordosis. These prolonged effects were independent of hormone treatment. (32 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Sequential inhibition of sexual behavior by progesterone in female rats: Comparison with a synthetic antiestrogen.

Findings from 6 experiments show that when a large dose of progesterone was administered to ovariectomized Sprague-Dawley rats 24 hrs after a 2-μg injection of estradiol benzoate (EB), sexual receptivity was inhibited at 54 hrs (sequential inhibition). Larger doses of progesterone (1 mg) were required to inhibit the induction of sexual receptivity when tested at 54 hrs than were necessary to facilitate at 30 hrs. This inhibition was not due to copulatory stimuli from the 1st test, because inhibition occurred even when the 1st test was omitted. The inhibition was dose dependent on estradiol; increasing the EB priming dose offset the inhibition caused by 1 mg of progesterone. The results of an experiment that behaviorally dissociated the antiestrogenic action of progesterone from that of a synthetic antiestrogen, CI-628, are consistent with the notion that progesterone and synthetic antiestrogens inhibit the neural effects of estradiol by separate mechanisms of action. (32 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effect of CNS depressants and stimulants on latency for the appearance of copulatory response in the female rat

Diethyl ether anesthesia, sodium hexobarbital (20 mg/kg), diphenylhydantoin (50 mg/kg), strychnine (1 mg/kg) and picrotoxin (1-0.25 mg/kg) effectively induced the copulatory response (lordotic behavior) in estradiol benzoate treated ovariectomized rats although no progesterone was given. As none of the tested compounds were effective in replacing progesterone in adrenalectomized animals, adrenal secretion is likely to be implicated in the lordosis activating effect of these compounds. The lordosis response appeared faster after the CNS stimulants than after treatment with the CNS depressants. The influence of diethylether anesthesia, strychnine (0.5 mg/kg) or picrotoxin (0.25 mg/kg) on the latency for the appearance of the lordosis response after IV injection of isopregnenone was studied in estradiol benzoate treated ovariectomized females. A 10 min ether anesthesia delayed the onset of the lordosis response in adrenal intact as well as adrenalectomized animals. Anesthesia given after receptivity had been fully established suppressed the responses for a short period (10-30 min) after the narcosis. The delay of the appearance of the first lordosis response after IV injection of isopregnone exceeded this period. Strychnine but not picrotoxin significantly shortened the latency to the onset of the female copulatory response. It is concluded that the lordotic activating action of progesterone or steroids with progesteronelike ability released from an endogenous source or given IV is influenced by compounds which exert a depressant or stimulant effect on neuronal activity. The total response obtained is not changed but the appearance of the response is prolonged by CNS depressants and shortened by certain CNS stimulants.     

Effects of hysterectomy on sexual receptivity, food intake, running wheel activity, and hypothalamic estrogen and progestin receptors in rats.

Ovariectomized-hysterectomized (OH) CD rats given sequential treatments with 2 μg of estradiol benzoate (EB) and .5 mg of progesterone (P) showed significantly higher lordosis quotients than ovariectomized (OV) Ss in 2 tests, 1 and 2 wks after surgery. To test whether the effects of hysterectomy persist, 3 groups of OV and OH Ss received weekly injections of EB, EB?+?P, or sesame oil for 4 wks, were given 2 μg of EB followed 24 hrs later by .5 mg of P, and tested for receptivity. Only the OH Ss that had received hormones for 4 wks showed a significantly higher lordosis score than OV Ss. The effects of hysterectomy on food intake, weight gain, and running wheel activity were also tested. After 1 wk of 2 μg/day EB, OH Ss lost significantly more weight and consumed less food than OV Ss, but by 2 wks the effects of hysterectomy were no longer evident. Treatment with .5 μg/day EB resulted in a significant loss in weight and food intake in OH Ss throughout the experiment. OH Ss implanted with Silastic capsules containing EB were significantly more active in running wheels than OV Ss over the 1st 9 days, but by Day 23 the activity of both groups was similar. 24 hrs following a single injection of EB, hypothalamic-preoptic area cell nuclear estrogen receptors and cytoplasmic progestin receptors were significantly higher in OH than in OV Ss. Possible mechanisms by which hysterectomy might act to enhance hormone-dependent behaviors are discussed. (20 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Regulation of female sexual behavior in the golden hamster: behavioral effects of mating and ovarian hormones

In the female hamster, sexual receptivity was abbreviated following copulation. Short-term effects of mating, lasting approximately 24-48 hr, were observed in females mated in either estradiol- or estradiol-and-progesterone-induced estrus. Long-term effects of copulation, of 9 days or more in duration, were apparent only in females chronically treated with both estradiol and progesterone, suggesting that progesterone exposure prolongs the inhibitory effects of mating. When progesterone stimulation was intermittent through the use of short-acting injection procedures, recovery from mating could be detected in 48 hr and was complete within 96 hr after copulation. The pattern of behavioral response to ovarian hormones in unmated females was also documented, replicating the "biphasic" effect of progesterone in this species. The inhibitory effects of mating and progesterone summate to produce consistent decrements in female sexual receptivity. It is postulated that short-term postcopulatory abbreviations in receptivity would reduce the vulnerability of the estrous female while long-term inhibitions, interacting with sustained progesterone stimulation, would reduce the probability of mating during pregnancy when hormone levels are elevated for a prolonged period.