Duration of hormonal deprivation: influences on physiological and behavioral responsiveness to estradiol

A total of 54 ovariectomized female guinea pigs were divided into three groups and tested six times at 2-week intervals for their responsiveness to exogenous ovarian hormones (3 days of 4 micrograms/kg estradiol benzoate plus 1 day of 0.4 mg/kg progesterone) or control injections (0.2 ml oil vehicle). Two weeks after ovariectomy, treatment with estradiol significantly reduced food intake and body weight, and also produced vaginal membrane rupture in 98.1% of the females. When tested for sexual behavior at 4, 6, and 8 hr after the progesterone injection, 29 of the subjects (53.7%) displayed lordosis in response to manual stimulation. Twelve weeks after ovariectomy, the effects of estradiol on food intake, body weight, and vaginal membrane condition had not diminished. However, the overall proportion of females from which lordosis could be elicited declined to 27.8%. Biweekly injections of estradiol benzoate plus progesterone to one of the groups of females did not prevent this decline in the sexual response. Based on these results, it was concluded that the observed reduction in behavioral lordosis does not represent a general decline in the responsiveness of ovariectomized guinea pigs to estrogenic stimulation, but may involve changes in their responsiveness to progesterone or in other mechanisms more specifically associated with sexual behavior.     

Appetitive and Consummatory Sexual Behaviors of Female Rats in Bilevel Chambers: I. A Correlational and Factor Analysis and the Effects of Ovarian Hormones

This study investigated measures of sexual behavior displayed by female rats in bilevel chambers, the statistical relationships among the measures, and their dependency on hormone priming. Normative data from a standard 35-min test of sexual behavior were gathered from 82 fully primed sexually experienced Long-Evans females and subjected to multiple correlational and factor analyses. Several consummatory measures of copulation were related significantly, whereas appetitive level changing was statistically independent of consummatory measures. Factor analyses were conducted using orthogonal rotations of correlational matrices derived either from (a) measures of female behavior alone or (b) measures of female and male behavior together. The first analysis revealed five factors that accounted for 84% of the intersubject variance: Receptivity, Pacing, Appetitive Level Changing, Lordosis Reflex, and Solicitation. The second factor analysis with male data included revealed seven factors that accounted for 95% of the intersubject variance: Pacing, Copulatory Rate, Mount Count, Receptivity, Appetitive Level Changing, Solicitation, and Lordosis Reflex. Subsequently, subsets of these females were maintained on different steroid priming regimens (oil, low estrogen, high estrogen, high estrogen and progesterone) prior to a standard test of sexual behavior. Although the expression of all sexual behaviors required estrogen priming, appetitive level changing, solicitation, and pacing required progesterone for their full expression. Finally, appetitive level changing developed following hormone treatment alone, regardless of whether the females received access to sexually active males, inactive castrated males, or other females. Use of bilevel chambers allows complex patterns of sexual behavior to be observed in female rats and may thus facilitate the identification of neurochemical or endocrine mechanisms associated with different aspects of female sexual motivation and performance.     

Bisexual behavior in the male rat: Influence of masculine sexual activity on the display of lordosis behavior

Sexually inexperienced male Wistar rats (strain WI in our colony) known to very infrequently display spontaneous lordosis behavior (Schaeffer et al., 1990b) were used. A first group was tested four times at 5-day intervals for lordosis with vigorous stimulus males (heterotypic sexual behavior), immediately following testing for masculine sexual activity with highly receptive females (homotypic sexual behavior). A small number of animals displayed lordosis during the first test, but more and more animals displayed this behavior from the first to the fourth test. There was no relationship between the degree of masculine sexual activity--intromission without ejaculation or ejaculation--and the occurrence of lordosis behavior. A second group was tested only once for both masculine sexual activity and lordosis behavior as above and afterwards three times at 5-day intervals for lordosis behavior in the absence of any previous testing for masculine sexual activity. A few animals displayed lordosis during their first test. As compared to the first group, the animals which had not displayed lordosis in the first test never showed lordosis responses in the following tests. It is concluded that both homotypic and heterotypic sexual interactions are required for the display of lordosis behavior in the strain of Wistar rats used in this study.     

Protein synthesis in the medial preoptic area is important for the mating-induced decrease in estrus duration in hamsters

Sexual receptivity in female hamsters potentially lasts for about 16 h. However, vaginal cervical stimulation (VCS) from a male during mating eventually reduces receptivity and can shorten the duration of behavioral estrus. The process by which this change in response to the male takes place is unknown. Recently, detection of the Fos protein has indicated that the medial preoptic area (POA) is one of the brain regions particularly responsive to VCS. Additionally, the POA may have an inhibitory effect on sexual receptivity. To determine if protein synthesis in the POA is required to initiate the VCS-induced decrease in estrus duration, a protein synthesis inhibitor (anisomycin, 0.50 microg) or a control substance (cholesterol) was applied bilaterally to the POA of steroid-primed ovariectomized female hamsters. Females were tested with a sexually active male at five time points following the initial test for sexual receptivity (hour 1, 2, 6, 12, and 24). Half of the females tested were allowed to receive VCS from a male, while half were fitted with vaginal masks to prevent penile intromission. Each group receiving VCS showed a significant decrease in lordosis duration evident between hour 2 and hour 6, except the group which received anisomycin in the POA. In this respect the POA anisomycin group was similar to animals which did not receive VCS. Hamsters with vaginal masks and the anisomycin/POA animals allowed to receive VCS exhibited their first decrease in lordosis duration between hour 6 and hour 12. These results indicate that protein synthesis is important for VCS-induced decrease in estrus duration in the POA.     

Differential sensitivity of mounting and lordosis control systems to early androgen treatment in male and female hamsters.

The effects of early testosterone propionate (TP) treatment on the adult sexual behavior of hamsters were investigated in two experiments. In Expt. I, male and female pups were injected with oil vehicle or 1, 5, 10, 50, 100, or 250 μg of TP 24 hr after birth. In Expt. II, males and females received either oil or 10 μg of TP on the day of birth (Day 1), Day 3, Day 5, Day 7, or Day 9. At 70 days of age all animals were gonadectomized and 10 days later tested for lordosis behavior after estrogen and progesterone priming. One week after the test for female behavior all females began receiving 500 μg of TP each day and were tested for mounting and intromission behavior three times at 10 day intervals. Lordosis behavior was inhibited by as little as 5 μg of TP given 24 hr after birth. In males this dose produced the maximal effect, but in females increasing dosages resulted in a proportional decrease in lordosis duration. One μg of TP neonatally facilitated later mounting and intromission behavior in females and 250 μg of TP was no more effective than 1 μg. Lordosis duration was inhibited in females by 10 μg of TP on either Day 1 or 3, however, mounts and intromissions were facilitated by TP treatment on Day 1, 3, 5 or 7. These experiments demonstrate that the mechanisms mediating masculine behavior are more sensitive to neonatal TP treatment than are the mechanisms mediating lordosis behavior.     

Effects of naloxone and naltrexone on receptive and proceptive behaviors in female rats.

The sexual receptive and proceptive behaviors induced by opiate antagonists, naloxone and naltrexone in estrogen-primed ovariectomized rats were observed under the presence of sexually active males. The females were treated intraperitoneally with naloxone or naltrexone at doses ranging from 0.5 to 4.0 mg/kg and the sexual behavior of females was tested before and after the injection of drug. The results obtained suggest that the opiate antagonists play a role in the regulation of lordosis behavior, but not proceptive behavior in female rats.     

Differential hormonal control of aggression and sexual behavior in female Syrian hamsters

These experiments were designed to test the effects of chronic estradiol treatment on aggression and sexual behavior in female hamsters. Isolated female hamsters were ovariectomized and tested for their behavioral responses to a group-housed, ovariectomized female hamster (aggression test) and a group-housed, intact male hamster (sexual behavior test). Following these baseline tests, the experimental females were implanted sc with Silastic capsules containing different concentrations of estradiol (100, 25, 10, or 0%) diluted with cholesterol and retested 3, 7, 10, and 14 days after implantation. High levels of aggression were observed on the baseline test, with no changes in aggression toward an intruder female observed for any implant group on subsequent tests. Despite these high levels of aggression toward another female, most of the estradiol-treated females (80% at 14 days) were sexually responsive in the presence of a male. There was no effect of Silastic estradiol concentration on sexual behavior, even though a range of serum estradiol levels (39–105 pg/ml) resulted. Lordosis latencies decreased and lordosis durations increased over the extent of estradiol treatment. Seventeen days after Silastic implantation, all females were injected with progesterone and retested. Estradiol-treated females showed an extreme reduction in aggression toward a stimulus female, as well as a further stimulation of sexual behavior after progesterone treatment. High levels of aggression in cholesterol-treated females (0% estradiol) were maintained even after progesterone injection, and these females never displayed any sexual responsivity. These results suggest that sexual behavior in the female hamster is sensitive to estradiol alone, whereas the inhibition of aggression requires the combination of estradiol plus progesterone.     

Progesterone facilitation of lordosis in male and female Sprague-Dawley rats following priming with estradiol pulses

Adult male Sprague-Dawley rats rarely exhibit progesterone-facilitated lordosis following steroid treatments which are effective in females. In contrast, progesterone-facilitated lordosis has been observed following priming with estradiol pulses in another strain. The aim of this study was to compare progesterone-facilitated feminine sexual behavior in adult male and female Sprague-Dawley rats following priming with estradiol benzoate (EB) or estradiol pulses. Female sexual behavior was measured in adult, gonadectomized males and females treated as follows: Two pulses of estradiol followed by progesterone or oil the next day; EB (two doses) for 3 days, and progesterone or oil the next day. These protocols were repeated at 4- or 6-day intervals, respectively. Progesterone-facilitated lordosis was observed consistently in both sexes treated with estradiol pulses. By the fifth test, lordosis quotients did not differ between the sexes, but the lordosis ratings in progesterone-treated males remained lower than those observed in females. Proceptivity (hop-darting) was facilitated by progesterone in females, but was never observed in males. Lordosis was induced in both sexes by 15 micrograms EB, but was not reliably facilitated by progesterone. Treatment with the lower dose of EB (1.5 micrograms) induced high levels of receptivity in females (occasionally facilitated by progesterone), but not in males regardless of subsequent treatment (i.e, progesterone or oil). These data suggest that progesterone-facilitated lordosis can be induced in male Sprague-Dawley rats, if a regimen of estradiol pulses is used. Thus, the brain of the adult male is not inflexibly differentiated with regard to progesterone facilitation of feminine receptive behavior.     

Role of postnatal androgens in sexual differentiation of the lordosis-inhibiting effect of central injections of cholecystokinin

The neuropeptide cholecystokinin (CCK) inhibits lordosis behavior when infused into the ventromedial nucleus of the hypothalamus (VMN) of female rats and has no effect when infused into the VMN of male rats. To test whether this sex difference develops under the control of perinatal steroids, male rats were castrated or given sham surgeries within 3 h of birth and female rats were injected with either 0 or 100 micrograms testosterone propionate on postnatal day 5. As adults, these rats were castrated as necessary, implanted with unilateral cannulae directed at the VMN, and tested for their ability to display female sexual behavior and to respond to CCK. Neonatal castration of males prevented defeminization of this response. When treated with 5 micrograms estradiol benzoate (EB), neonatally castrated males showed both lordosis behavior and a profound inhibition of that behavior after infusions of CCK. Neonatally castrated males did not display lordosis behavior when treated with 2 micrograms EB. Control males showed no lordosis behavior and, therefore, no response to CCK. Both doses of EB induced lordosis behavior in neonatally androgenized females. Significantly, these neonatally androgenized females were less responsive to CCK's inhibition of lordosis and were also anovulatory. These results imply that androgens alter the development of CCK responsive circuits as well as defeminize cyclic gonadotropin release. Levels of 125I-sCCK-8 binding in the VMN were correlated closely with an individual's ability to respond to sCCK-8. In summary, the inhibition of female sexual behavior caused by exogenously administered CCK in normal adult female rats appears to be controlled at least partially by levels of CCK receptors in the VMN and to differentiate under the control of perinatally present testosterone.     

Lordosis behavior in castrated male rats treated with estradiol benzoate or testosterone propionate in combination with an estrogen antagonist, MER-25, and in intact male rats

Lordosis behavior could be elicited by manual stimulation in castrated male rats after treatment with estradiol benzoate (15 μg for 10 days) or testosterone propionate (1 or 3 mg for 10 days). The effect was antagonized by treatment with the estrogen antagonist MER-25 (10mg for 10 days). Prolonged treatment with testosterone propionate (1 mg for 26 days) resulted in display of male (nine of ten rats) as well as female (seven of ten rats) sexual behavior. Eleven of 32 intact male rats (age 120 days) and 22 of 37 other intact males (age 75 days) displayed lordosis in response to manual stimulation without hormonal treatment. Seven intact males which showed lordosis without hormone treatment were injected with MER-25 (10 mg/day × 10 days) and lordosis was abolished in six cases. The results suggest that estrogen is involved in the regulation of lordosis behavior in TP-treated and intact male rats.     

Mu-, delta-, and kappa-opioid receptor agonists selectively modulate sexual behaviors in the female rat: differential dependence on progesterone.

Previous studies suggested that opioid receptor agonists infused into the lateral ventricles can inhibit (through mu receptors) or facilitate (through delta receptors) the lordosis behavior of ovariectomized (OVX) rats treated with estrogen and a low dose of progesterone. The present study investigated the behavioral and hormonal specificity of those effects using more selective opioid receptor agonists. Sexually experienced OVX rats were implanted stereotaxically with guide cannulae aimed at the right lateral ventricle. One group of rats was treated with estradiol benzoate (EB, 10 micrograms) 48 hr and progesterone (P, 250 micrograms) 4 hr before testing, whereas the other group was treated with EB alone. Rats were infused with different doses of the selective mu-receptor agonist DAMGO, the selective delta-receptor agonist DPDPE, or the selective kappa-receptor agonist U50-488. The females were placed with a sexually vigorous male in a bilevel chamber (Mendelson and Gorzalka, 1987) for three tests of sexual behavior, beginning 15, 30, and 60 min after each infusion. DAMGO reduced lordosis quotients and magnitudes significantly in rats treated with EB and P, but not in rats treated with EB alone. In contrast, DPDPE and U50-488H increased lordosis quotients and magnitudes significantly in both steroid-treatment groups. Surprisingly, measures of proceptivity, rejection responses, and level changes were not affected significantly by mu or kappa agonists, although proceptivity and rejection responses were affected by DPDPE treatment. These results suggest that the effects of lateral ventricular infusions of opioid receptor agonists on the sexual behavior of female rats are relatively specific to lordosis behavior. Moreover, the facilitation of lordosis behavior by delta- or kappa-receptor agonists is independent of progesterone treatment, whereas the inhibitory effect of mu-receptor agonists on lordosis behavior may require the presence of progesterone.     

Independence of the differentiation of masculine and feminine sexual behavior in rats.

Male rats received Silastic implants of the aromatase inhibitor, 1,4,6-androstatriene-3, 17-dione (ATD), on days 2–10 of life. Controls received blank implants. There were no differences in the masculine sexual behavior of ATD and control males when they were tested as gonadally intact adults. In contrast, even without exogenous hormone treatment, nine of 14 ATD males exhibited lordosis behavior, whereas only one of 12 controls did so. In addition, during a sexual preference test in which access was provided to both a sexually receptive female and to a stud male, there was no difference in the proportions of ATD ($\text{11}\text{14}$) and control ($\text{7}\text{12}$) males that copulated with the stimulus female; however, seven of the ATD males also exhibited feminine sexual behavior including some instances of solicitation. Only one of the control males showed any lordosis behavior. In general, all animals spent more time with the stimulus female than with the stud male. At the termination of preference testing, all animals were castrated and then tested twice for feminine sexual behavior under exogenous estradiol benzoate and progesterone. All of the ATD males showed lordosis behavior with a mean lordosis quotient (LQ) of 85; and 11 of the 14 also showed solicitation behavior. Only five of 12 control males exhibited lordosis ($\text{X}\text{?}\text{LQ}\text{= 59}$) and only one showed solicitation behavior. These results indicate that the propensity of males to show feminine sexual behavior can be manipulated independently of the capacity for masculine sexual behavior. Moreover, our results suggest that the process of defeminization may occur primarily postnatally in rats since treatment during that period results in substantial increments in later feminine sexual behavior including solicitation behaviors.     

Effects of neonatal septal lesions on reproductive behavior of male and female rats

The purpose of this study was to examine the effects of neonatally placed septal lesions (SL) in male, female, and androgenized female rats on reproductive behavior. Animals were castrated as adults and tested for both feminine and masculine sexual behavior. After treatment with estradiol benzoate (EB) alone (2 μg daily for 3 days), only the females with SL which had not been given testosterone propionate (TP) neonatally showed a facilitation of lordosis behavior. Following EB (2 μg for 3 days) plus 0.5 mg progesterone (P), both the lesioned and the sham-operated female groups showed an increase in the display of lordosis in either hormonal condition. All animals were given a pretest for masculine sexual behavior and tested on Days 4, 7, 11, and 15 of daily TP treatment (150 μg/day). There was no effect of the neonatally placed SL on masculine sexual behavior in female rats or in female rats androgenized with 30 μg TP. However, lesioned females treated neonatally with 1 mg TP showed a marginal enhancement of masculine sexual behavior. Male rats given SL neonatally showed a marked enhancement of masculine sexual behavior compared to that of controls. These results suggest that, depending on the neonatal hormone environment, SL selectively increase behavioral sensitivity to hormones. Although neonatally lesioned females show behavioral responses similar to females given SL as adults, male rats given SL neonatally are unique in that they show enhanced masculine sexual behavior whereas males lesioned as adults do not.     

Facilitatory and inhibitory effects of beta-endorphin on lordosis in female rats: relation to time of administration.

The purpose of the present study was to investigate the effect of time of beta-endorphin (beta-EP) administration on lordosis in ovariectomized female rats injected subcutaneously (sc) with estradiol benzoate (EB) and progesterone (Prog). Intracerebroventricular (icv) injections of beta-EP and naloxone (NLX), an opioid receptor antagonist, were administered at the various stages of sc steroid hormone priming. Facilitation of lordosis induced by 10 microg beta-EP was observed exclusively within the initial 6 h of estrogen action, after which inhibition of lordosis occurred. At 12 h after EB priming, at the time of sc Prog treatment (or 43 h after EB priming), icv injection of 10 microg beta-EP significantly inhibited lordosis. Lordosis was significantly facilitated by icv injections of 1 and 10 microg beta-EP at the time of sc EB priming, but not by 0.1 microg beta-EP. A dose-response relationship was identified for lordosis in experimental animals receiving icv injection of beta-EP. Lordosis was inhibited by icv injections of 1 and 10 microg beta-EP at 1 h before the test (or 47 h after EB priming). Lordosis was significantly inhibited by icv injection of NLX at all stages. From the present results, it seems that two different mechanisms are involved in endorphinergic modulation of rats' sexual receptivity: (a) the endorphinergic system at the initial stages of estrogen action facilitates the estrogen activation of lordosis; (b) the endorphinergic system at the final stages of steroid action inhibits lordosis. Moreover, there exists a critical time between 6 and 12 h after estrogen priming for endorphinergic mediation to modulate estrogen action.     

Vaginocervical stimulation induces Fos in glutamate neurons in the ventromedial hypothalamus: Attenuation by estrogen and progesterone

Vaginocervical stimulation (VCS) induces the immediate-early gene product Fos in the ventromedial hypothalamus (VMH) of female rats. However, this induction is lower in ovariectomized rats that receive estradiol benzoate (EB) and progesterone (P) relative to an oil vehicle. We have observed that a substantial proportion of cells activated in the VMH by VCS stain for glutamate, and infusions of glutamate or its selective receptor agonists to the VMH inhibit both appetitive and consummatory sexual behaviors in females. This raises the possibility that VCS activates an inhibitory glutamate system in the VMH, and that ovarian steroids blunt the activation, although it is not known whether EB or P, alone or in combination, lead to this effect. The present experiment examined the ability of VCS to induce Fos in glutamate neurons in the VMH of ovariectomized rats under 4 hormonal regimens: oil, EB alone, P alone, or EB + P, following 1 or 50 distributed VCSs administered with a lubricated glass rod over the course of 1 h. Treatment with EB or P alone significantly reduced the number of glutamate neurons activated by 1 VCS, with P being more effective than EB. Treatment with EB + P also produced a significant reduction, but not to the extent of EB or P alone. Although EB and P work in synergy to activate sexual behavior in female rats, actions of EB or P alone are sufficient to blunt the ability of VCS to activate glutamate neurons in the VMH. It thus appears that ovarian steroids may “disinhibit” sexual responding, in part, by dampening the ability of VCS to activate glutamate neurons in the VMH. In turn, this may allow females to receive a sufficient number of intromissions for the activation of sexual reward and the facilitation of pregnancy.     

Progesterone-Facilitated Lordosis in Medial Preoptic Area-Lesioned, Juvenile Guinea Pigs

Juvenile female guinea pigs rarely display lordosis in response to estradiol and progesterone treatments that elicit sexual receptivity in adults. To test the hypothesis that the medial preoptic area (MPOA) tonically inhibits the display of steroid-induced lordosis in juveniles, 11-day-old guinea pigs were ovariectomized (OVX) and received bilateral, sham, or electrolytic lesions aimed at the MPOA 3–4 days later. At 20–22 days of age, these females were tested for the expression of sexual receptivity following injections of estradiol benzoate (EB, 10 μg sc) and progesterone (0.5 mg sc, 40 h after EB). The lesions damaged portions of the MPOA, the nucleus of the diagonal band of Broca, the lateral aspect of the medial preoptic nucleus, the medial part of the preventricular portion of the periventricular nucleus, and the anterior commissure. The lesions did not alter the display of estradiol-induced lordosis. However, after treatment with EB plus progesterone, 20% of the sham-lesioned females displayed lordosis, as compared to 80% of the MPOA-lesioned animals. These data are consistent with the hypothesis that neurons originating in and/or traversing the MPOA tonically suppress the display of progesterone-facilitated lordosis in juvenile guinea pigs. Removal of this inhibitory input allows prepubertal females to respond behaviorally to estradiol and progesterone in an adult-typical fashion.     

Paced mating behavior in female rats in response to different hormone priming regimens

A female rat will display a repertoire of behaviors during a sexual encounter with a male rat including sexually receptive (the lordosis response) and proceptive (hopping, darting) behaviors. In addition, when given the opportunity, a sexually receptive female rat will approach and withdraw from the male rat, controlling the timing of the receipt of mounts, intromissions, and ejaculations, a behavior known as paced mating behavior. The present experiments tested the hypotheses (1) that progesterone regulates paced mating behavior, and (2) that multiple hormone regimens used previously to induce sexual receptivity have the same effect on paced mating behavior. Paced mating behavior was assessed in sexually receptive ovariectomized female rats after treatment with: (1) estradiol benzoate (EB; 30.0 mg/kg) followed by a range of doses of progesterone (P; 1.0-8.0 mg/kg), (2) two pulses of unesterified estradiol (E2; 2.0 microg/rat) followed by 1.0 mg/rat of P, and (3) EB alone (5.0 microg/rat) for 6 days. No differences in sexual receptivity or in paced mating behavior were observed across doses of P (1.0-8.0 mg/kg). In contrast, the number of hops and darts per min increased with the dose of P administered. E2 + P administration resulted in slightly, but significantly, lower levels of sexual receptivity along with significantly longer contact-return latencies following an intromission in relation to the other treatment conditions. In addition, female rats exhibited fewer hops and darts per min in response to E2 + P than in response to EB + 8.0 mg/kg of P. The administration of EB alone for 6 days induced levels of receptivity and paced mating behavior indistinguishable from EB + P, while eliciting significantly fewer hops and darts per min than the EB + 8.0 mg/kg P treatment condition. Hormone priming regimen had no effect on the percentage of exits displayed during the paced mating tests in any experimental phase. Dose of P had no effect on paced mating behavior in sexually receptive rats. In addition, P does not appear to be necessary for the display of paced mating behavior following long-term treatment with EB. In contrast, the pulsatile administration of E2 + P induced a different pattern of paced mating behavior in sexually receptive rats.     

Effects of septal lesions on behavioral sensitivity of female rats to gonadal hormones

Spayed female rats were given bilateral septal lesions or a sham operation and 3 wk later tested for hormone-induced female sexual behavior. When primed with 0.5, 1.0, or 2.0 μg of estradiol benzoate (EB) per day for 3 days and tested for lordosis behavior on the fourth day, animals with septal lesions showed a positive dose-related increase in mean lordosis quotient (LQ), whereas control animals showed a low mean LQ for all doses of EB. After priming with a low dose of EB (0.5 μg/day for 3 days), progesterone administration prior to behavior testing on day 4 produced a comparable facilitation in LQ for both septal-lesioned and sham-operated animals. When treated for 3 days with either 50 or 150 μg of testosterone propionate (TP) and given progesterone prior to behavior testing on day 4, female rats with septal lesions showed a higher mean LQ than sham-operated rats. Thus, septal lesions increase the behavioral sensitivity of female rats to both EB and TP as measured by female sexual behavior, but do not appear to alter the responsiveness of animals to progesterone.     

Accumbens lesion in female rats increases mount rejection without modifying lordosis

Ovariectomized Wistar rats received bilateral electrolytic (n = 24) or sham (n = 11) lesion of the nucleus accumbens. Following priming with estradiol benzoate (25 micrograms/rat) and progesterone (0.5 mg/rat) they were tested for sexual behavior with a stud male. Tests were carried out once prior to operation and twice postoperatively. Both lordosis and rejection behaviors as responses to male mount attempts were evaluated for each session. Proceptive patterns (hopping, darting and presenting) were also recorded. Females with accumbens lesion did not differ from control animals either with regard to lordosis or to soliciting behaviors. On the contrary, the lesioned group showed a statistically significant increase in rejection behavior in both postoperative sessions (p less than 0.05 and p less than 0.002). In conclusion, nucleus accumbens lesion dissociated the normal correlation between lordosis and rejection responses to male mount attempts without affecting soliciting behaviors. This finding is thought to be related to the hyperreactivity produced by nucleus accumbens lesion.     

Vaginocervical stimulation attenuates the sensitization of appetitive sexual behaviors by estradiol benzoate in the ovariectomized rat

The acute administration of estradiol benzoate (EB) to the ovariectomized (OVX) rat induces low levels of lordosis while sexually appetitive behaviors (e.g., hops, darts, solicitations) are absent, yet the repeated administration of EB results in a behavioral sensitization in which lordosis is potentiated and sexually appetitive behaviors are induced. We have shown that repeated copulation attenuates the sensitization of appetitive sexual behaviors. Here, we assessed which component of male stimulation during copulation is involved in the attenuation. On 8 occasions, sexually experienced OVX Long–Evans rats were treated with 10 μg EB and 48 h later assigned to one of six groups that differed in their experience on intermediates tests (2–7). One was given repeated access to a male (EB/Male), and another was placed in the copulation chamber alone (EB/Alone) on intermediate tests. Three groups were given one of three somatosensory stimuli by the experimenter: manual flank stimulation (FLS), clitoral stimulation (CLS), or vaginocervical stimulation (VCS). Finally, the control group was left undisturbed in the animal care facility (ACF). Sexual behaviors were measured on Tests 1 and 8. VCS received from the experimenter (VCS) or from the male during copulation (EB/Male) attenuated the magnitude of the sensitization of appetitive sexual behaviors compared with those that were not brought to the testing rooms (ACF), and the effect was most pronounced on sexual solicitations. These results suggest that VCS received during penile intromission inhibits the sensitization of sexually appetitive behaviors by repeated administration of EB. As such, repeated administration of EB may oppose those mechanisms that induce estrous termination, perhaps by sensitizing inhibitory processes within the ventromedial hypothalamus that typically prevent the display of sexual behaviors (i.e., by facilitating disinhibition).