Lordosis behavior in intact male rats: effects of hormonal treatment and/or manipulation of the olfactory system

The aim of this study was to investigate the olfactory mechanisms regulating the display of lordosis behavior in intact Wistar male rats bred in our colony. Gonadally intact males show a low capacity to respond by lordosis to male mounts and were insensitive to manipulations of the olfactory system (exposure to the odor of male urine or accessory bulb removal (AOBR)) which have been previously shown to facilitate the display of lordosis behavior in orchidectomized animals primed with ovarian hormones. Treatment with either estradiol benzoate (EB) or EB and progesterone (P) consecutively did not render these gonadally intact animals sensitive to the effects of AOBR. By contrast exposure to male urine was capable of facilitating the display of lordosis behavior in intact male rats given EB + P consecutively. These results are discussed in the light of previous findings showing that (1) two inhibitory structures, the accessory olfactory bulb and the septal and preoptic areas, are involved in the control of lordosis behavior in the male rat; (2) the effects of olfactory cues on the display of lordosis behavior are dependent on the action of both EB and P in orchidectomized animals.     

Effects of septal lesions on the lordotic behavior of weanling male and female rats

Twenty-four-day-old weanling male and female rats were either lesioned in the septal area, gonadectomized, lesioned and gonadectomized, or not treated. Tests for lordotic behavior were carried out at 27 and 28 days of age after priming with estradiol alone and with estradiol plus progesterone. A second set of tests for lordotic behavior was carried out at 47 and 48 days of age. In the interim period, some of the animals were given chronic estrogen treatment. In tests given at 27 days of age, septal lesions facilitated lordotic responding after estrogen priming; no differences were observed between male and female animals. At 47 and 48 days of age, however, unless male rats had been exposed to chronic estrogens following septal lesioning, no facilitation of estrogen-induced lordotic behavior occurred. In addition, it was found that female rats gonadectomized at 24 days of age and given no exposure to estrogens between the tests at 27 and 28 days and those at 47 and 48 days of age showed reduced sensitivity to estrogens, as compared to normal or estrogen-treated females, whether lesioned or not.     

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.     

Septal lesions: effects on lordosis behavior and pattern of gonadotropin release

Septal lesions increase behavioral responsiveness to estrogen of male, female, and androgen-sterilized female (ASF) rats as measured by lordosis behavior. Male and ASF animals normally show low levels of female sexual receptivity when compared to normal female rats. However, the level of female sexual behavior in male and ASF rats with septal lesions is comparable to that of highly receptive female rats. Progesterone facilitates the estrogen-induced female sexual behavior of female, but not male or ASF, animals. Andrenalectomy had no effect on the increased behavioral sensitivity to estrogen induced by septal lesions. Amygdala lesions, comparable in size to septal lesions, did not facilitate female sexual behavior. The male or female pattern of gonadotropin release is not affected by septal lesions, indicating a disassociation between the regulation of gonadotropin release and sexual behavior. Since septal lesions facilitate lordosis behavior in rats, the septal region appears to exert a tonic inhibition on female sexual behavior.     

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.     

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.     

Estrogen and progesterone interactions influencing sexual and social behavior in the brown lemming, Lemmus trimucronatus.

The effects of estrogen and progesterone on the social and sexual behavior of brown lemmings, Lemmus trimucronatus, were investigated. The behavior of hormone-treated and untreated ovariectomized females and sexually vigorous males was observed in six consecutive daily 5-min dyadic encounters. Sexual receptivity, as measured by lordosis, and other social behaviors including nasonasal contact, boxing postures, allogrooming, perineal investigation, and male mounting increased following 48 hr of exposure to daily injections of 0.5 μg estradiol benzoate (EB). Lordosis in EB-primed females was not facilitated or inhibited by short-term (4 hr) exposure to 0.5 mg progesterone (P). Long-term (greater than 24 hr) exposure to P apparently inhibited lordosis and other social behaviors in EB-treated females, although males continued to attempt to mount these females. In EB-treated females a dramatic increase in threat-leaps, directed by the female toward the male, was observed within 4 hr of P injection. Threat-leaps declined when P was withdrawn. Threat-leaps were also observed in ovariectomized females after prolonged exposure to P only (0.5 mg/day). Vaginal perforation and cornification were first apparent 48 hr after EB injection. P-alone treated ovariectomized females also showed vaginal perforation but cornified cells were infrequent and these animals did not show lordosis.     

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.     

Induction of progestin receptors in the mediobasal hypothalamus of gonadally intact male rats primed with estrogen in relation to display of lordosis behavior

The purpose of this study was to determine whether the effects of estrogen on lordosis behavior in the male rat were related to the number of progesterone (P) receptors in the mediobasal hypothalamus (MBH) and/or dependent on blood P concentration. Two groups of gonadally intact male rats were given five successive doses of 1.0 or 2.5 micrograms estradiol benzoate (EB) and tested for lordosis behavior with a male stimulus at the end of the treatment. One month later they were again injected with EB and sacrificed under the same temporal schedule, but they were not tested for lordosis so as to prevent any emotionally stressful effects of intermale cohabitation. The males given 2.5 micrograms EB more frequently displayed lordosis responses to male mounts than those receiving 1 microgram EB, with a parallel increase in the number of MBH P receptors. The total number of MBH P receptors also appeared to be higher in the animals that displayed lordosis responses (lordosis group) than in those which did not (no lordosis group). In contrast, the display of lordosis behavior was negatively correlated with blood P concentration. Comparing MBH P receptors and blood P values in the EB treated and in nonhormonally treated gonadally intact animals which had been selected for either ability or inability to spontaneously display lordosis behavior, we observed that (1) EB was capable of increasing the number of MBH P receptors in the male rat; and (2) in the absence of EB treatment blood P values were higher in the animals showing lordosis than in those which did not. These data are discussed with respect to observations made in castrated male rats and in ovariectomized females.     

Endogenous progesterone and lordosis behavior in male rats given estrogen alone

Male rats castrated as adults were given successive doses of estradiol benzoate (EB) combined or not, with dexamethasone (DEXA) at the end of estrogen treatment. Two experiments were done to determine if progesterone (P) of adrenocortical origin was involved in the display of lordosis behavior under these experimental circumstances. There was a significant rise in blood P concentration in animals given 0.5 and 1.0 microgram EB when compared with oil-control injected animals, an effect which was completely suppressed by DEXA treatment. An increase in the proportion of estrogen treated animals displaying lordosis responses to male mounts was found with increasing doses of EB and paralleled the effects of EB on P adrenocortical secretion. However, the number of feminized animals given 1 microgram EB + DEXA was reduced to the level corresponding to the effects of 0.5 microgram EB on lordosis behavior. These data show that the secretion of P by the adrenals is involved in the expression of lordosis behavior in castrated male rats primed with repeated doses of estrogen.     

Inhibition of estrous behavior in rats by intrahypothalamic application of agents that disrupt nuclear binding of estrogen-receptor complexes

This study tested the hypothesis that estrogen facilitation of reproductive behavior in female rats requires the binding of estrogen-receptor complexes to the genomic components of hypothalamic cell nuclei. Female rats were implanted stereotaxically with bilateral guide cannulae aimed at the ventromedial nucleus of the hypothalamus (VMH). Animals were ovariectomized following recovery from the implant surgery and randomly assigned to receive one of four drug treatments: actinomycin-D, ethidium bromide, netropsin, or 4', 6-diamidino-2-phenylindole. Each female received at least two tests for estrous behavior 48 hr after estrogen priming. On one test, drug-filled cannulae were lowered into the VMH 1 hr prior to a subcutaneous injection of 2-3 micrograms of estradiol benzoate (EB); on the other test blank cannulae were inserted 1 hr prior to EB treatment. Intracranial administration of all four compounds, which disrupt estrogen-receptor binding to hypothalamic nuclei, inhibited both the quantity and the quality of lordosis responses to systemic injections of EB. The results support the hypothesis that specific receptor interactions with the genome of hypothalamic cells mediate estrogen facilitation of estrous behavior in female rats.     

Androgen- and estrogen-induced copulatory behavior and inhibition of luteinizing hormone (LH) secretion in the male rat

The purpose of the present investigation was to determine if estrogen, aromatizable androgen or nonaromatizable androgen is capable of (1) inducing copulatory behavior and (2) inhibiting the postcastration rise in plasma LH. Castrate male rats were injected daily with either 1 mg testosterone (T), androstenedione (A), dihydrotestosterone (DHT), or 25 μg estradiol benzoate (EB) or oil and tested weekly for masculine behavior and for lordosis behavior after 38 days of steroid treatment. On day 40 blood was collected for radioimmunoassay of plasma LH. At least 89% of the males treated with T, A, or EB and 55% of those treated with DHT displayed ejaculatory behavior whereas none of the oil-treated males showed male copulatory behavior. Only estrogen-treated males displayed lordosis behavior. T and to a lesser extent A treatment reduced high levels of plasma LH; however, DHT and EB further reduced plasma LH to undectable levels. The relative potency of the steroid effect in stimulating accessory sex tissues followed the order: DHT > T > A > EB = oil. Significant dissociation was observed between the effects of these steroids on peripheral morphology, negative feedback, and mating behavior. These results indicate that masculine behavior is facilitated to the greatest extent, although not exclusively, by centrally acting aromatizable androgen or estrogen, whereas under the present conditions only estrogen stimulates feminine behavior.     

The reversible inhibition of steroid-induced sexual behavior by intracranial cycloheximide

Cycloheximide(Cyclo), an inhibitor of protein synthesis by a direct action on protein synthesis at the ribosomal level, was used to reversibly inhibit estrogen-induced sexual receptivity. Cyclo (100 μg per rat) was infused into the preoptic area(POA) of ovariectomized rats at varying times before, simultaneously with, and after 3 μg of subcutaneous estradiol benzoate (EB). All animals received 0.5 mg progesterone (P) 36 hr after EB, and were tested for sexual receptivity 4–6 hr after P. The females were placed with stud males and a lordosis quotient was computed for each female (lordosis quotient = number of lordosis responses/20 mounts by the male × 100). Females receiving Cyclo 6 hr before, simultaneously with, or 12 hr after EB showed significantly lower levels of sexual receptivity when compared to females receiving Cyclo 36 hr before and 18 and 24 hr after EB. When those animals that showed low levels of sexual behavior after Cyclo infusion were reprimed with EB and P 7 days later and presented with a male they showed high levels of sexual receptivity. Thus, the effect of Cyclo was reversible. Only Cyclo infusions into the POA (bilateral) and third ventricle were effective in suppressing sexual behavior. Caudate nucleus, lateral ventricle, and unilateral POA infusions were without effect.The data presented are in agreement with earlier work that utilized actinomycin D to inhibit steroid-induced sexual behavior. Cyclo was found to be less toxic than actinomycin D. All of the available evidence is consistent with the hypothesis that estrogen stimulates RNA and/or protein synthesis in its facilitation of sexual behavior in the female rat.     

A re-examination of the lordosis response in female rats given high doses of testosterone propionate or estradiol benzoate in the neonatal period

High lordosis quotients (LQ) were observed when female Wistar rats injected with 1.25 mgm of testosterone propionate (TP) on Day 4 of postnatal life were tested as intact adults. The high LQ was not due to testing during the lights-on period, the age at which the females were tested, the use of a strain that was insensitive to the masculinizing action of TP or estradiol benzoate (EB), the age at which the females were injected with TP or EB, or an abnormal response to estrogen. High LQ values were found in similar tests on adult female rats of two other strains injected with 1.25 mgm TP on Day 4 of life. A marked reduction of the facilitatory action of progesterone on receptivity in estrogen-primed animals was demonstrated in the females of all three strains treated with TP or EB during the neonatal period and for males after castration as adults.Analysis of the experimental records of the mating tests showed that females anovulatory following TP or EB administration during the neonatal period and tested either intact and under the influence of endogenous hormones or under the influence of exogenous estrogen showed a rapid and highly significant increase in receptivity during the course of prolonged (20 min) tests with two or three active stimulus males. This effect was very much reduced if the treated females were under the influence of exogenous estrogen plus progesterone. The effect was not seen in males castrated as adults and treated with estrogen, or in females not treated with steroids in the neonatal period and tested intact at proestrus alone or under the influence of exogenous steroids after ovariectomy. A significant increase in LQ during the test period was observed in females of the Wistar strain which were anovulatory as a result of exposure to constant light and were tested intact without any exogenous hormone being administered.It is suggested that although tests involving a limited number of mounts or attempts to mount at low rates over a short period of time may be adequate to determine the degree of receptivity of normal female rats they are not adequate to establish the capacity of female rats treated with steroid hormones during the neonatal period to display the lordosis response.     

Estrogen and progesterone dose-dependently reduce disruptive effects of restraint on lordosis behavior

Ovariectomized rats were hormonally primed with various doses of estradiol benzoate (EB; 0.5-10 microg) in combination with various doses of progesterone (2.5-500 microg) to induce sexual receptivity. Females were then subjected to 5 min restraint and the effect on lordosis behavior was monitored for the next 30 min. Such mild stress has been previously shown to transiently reduce lordosis behavior of ovariectomized females hormonally primed only with 10 microg EB. In the current study, doses of progesterone of 25 microg or more in combination with 10 microg EB reduced the effects of restraint. Also priming doses of EB from 4.0 to 10 microg in combination with 250 microg progesterone prevented the lordosis-inhibiting effects of restraint. These findings reinforce prior observations of the dose-dependency of both estrogen and progesterone in the facilitation of lordosis behavior and introduce the female's lordosis response to mild restraint as a potentially useful index of the female's response to stress.     

Differential effects of the anti-estrogen MER-25 and of three 5alpha-reduced androgens on mounting and lordosis behavior in the rat.

Four experiments were performed in order to evaluate further the hypothesis that androgen must be aromatized to estrogen for the activation of masculine sexual behavior in the male rat. In Experiment 1 it was found that the anti-estrogen MER-25 failed to disrupt mounting behavior in castrated males which simultaneously received testosterone propionate (TP). However, in Experiment 2 it was found that MER-25 as weil as 3β-androstanediol effectively activated masculine behavior in castrated males treated simultaneously with dihydrotestosterone propionate. Both MER-25 and 3β-androstanediol had previously been shown to display an affinity for cytoplasmic estradiol-17β receptors present in male rat anterior hypothalamus. In Experiments 3 and 4, performed with ovariectomized females, it was found that whereas MER-25 antagonized the stimulatory effect of estradiol benzoate (EB) on lordosis behavior, 3β-androstanediol did not. In addition, 5α-dihydrotestosterone and 3α-androstanediol, two compounds which had previously been shown to have almost no affinity for estradiol-17β receptors in the hypothalamus, both inhibited the stimulatory effect of EB on lordosis. It is concluded that the fact that anti-estrogens suppress lordosis induced in females with either EB or TP, but fail to disrupt TP-induced mounting behavior in male rats does not argue against the aromatization hypothesis for masculine sexual behavior.     

Induction of male mating behavior in androgen-insensitive (tfm) and Normal (King-Holtzman) male rats: effect of testosterone propionate, estradiol benzoate, and dihydrotestosterone

Castrated androgen-insensitive rats exhibited mounting and intromission patterns in response to testosterone propionate (TP), estradiol benzoate (EB), or EB combined with dihydrotestosterone (DHT) treatment in adulthood. Treatment with DHT alone was ineffective in stimulating male mating behavior in the mutant rats. Since androgen-insensitive rats, like normal males, have the potential to show mounting behavior following hormone treatment in adulthood, the neural substrate underlying this behavior must be masculinized during development. The effectiveness of gonadal hormones in activating the entire copulatory sequence in castrated littermate males (King-Holtzman) was also examined. TP treatment induced mating behavior in the control rats. DHT also stimulated the complete copulatory pattern, although it was not as effective as TP. The administration of EB, however, did not induce ejaculation in control rats. These results do not support the hypothesis that the activation of male mating behavior by testosterone requires its metabolite estrogen (aromatization hypothesis).     

Inhibition of estrogen facilitation of sexual behavior by the intracerebral infusion of actinomycin-D

It has been shown previously that intracerebral actinomycin-D (Act-D) pellets inhibit estrogen facilitated female sexual behavior, but it was not possible to test the reversibility of this effect. In the present study an attempt was made to distinguish between the possible temporary interruption by Act-D of the biochemical action of estrogen which facilitates sexual receptivity and permanent toxic effects of the drug. Act-D in saline was infused into the third ventricle or the preoptic area (POA) to determine whether a reversible suppression of sexual behavior as measured by the lordosis quotient (LQ) could be produced. Ovariectomized rats were implanted with midline guide tubes entering the third ventricle (eight rats) or with bilateral tubes extending to the corpus callosum above the POA (67 rats). Each animal served as its own control since pretest and Act-D and recovery tests were performed 10–14 days apart in most subjects. For each behavioral test implanted subjects were primed with 3μg estradiol benzoate (EB) and 0.5 mg progesterone (P) 48 hr later. Behavioral tests, each involving 50 mounts, were performed 4–6 hr after P. Following the pretest the animals were retested under experimental conditions. Inner cannulae were inserted into the POA through the guide tubes and 0.11 μg Act-D infused 24 or 12 hr before, simultaneously with, or 6, 12, 18, or 26 hr after EB. A recovery test was performed 10–14 days later with no intracerebral infusion. The control procedure (infusion of of saline either simultaneously with or 12 hr after EB) did not alter the LQ. Act-D infusion produced a reversible suppression of lordosis which was dependent upon the time of administration of Act-D. Intraventricular infusion of Act-D 6 hr after EB reversibly inhibited lordosis behavior and no lesions were produced. Act-D infused into the POA simultaneously with EB or 6 hr later reversibly suppressed the LQ. In the 6 hr group, for example, the LQ fell from 78.3 to 35.7, but 10–14 days later reached 74.3. Although brain lesions of varying extent were produced by Act-D, the marked but reversible suppression of lordosis behavior is consistent with the view that Act-D inhibits estrogen facilitation of lordosis behavior by means of a biochemical rather than cytotoxic action.     

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.     

Gonadal hormones masculinize and defeminize reproductive behaviors during puberty in the male Syrian hamster

Three experiments were conducted to test whether testicular hormones secreted during puberty masculinize and defeminize the expression of adult reproductive behavior. Experiment 1 tested the hypothesis that gonadal hormones during puberty masculinize behavioral responses to testosterone (T) in adulthood. Male hamsters were castrated either before puberty (noTduringP) or after puberty (TduringP). All males were implanted with a 2.5-mg T pellet 6 weeks following castration and tested once for masculine reproductive behavior 7 days after the onset of T replacement. TduringP males displayed significantly more mounts, intromissions, and ejaculations than noTduringP males. Experiment 2 tested the hypothesis that gonadal hormones during puberty defeminize behavioral responses to estrogen (EB) and progesterone (P). Eight weeks following castration, noTduringP and TduringP males were primed with EB and P and tested for lordosis behavior with a stud male. Behavioral responses of males were compared to that of ovariectomized (OVX) and hormone primed females. NoTduringP males and OVX females displayed significantly shorter lordosis latencies than TduringP males. Experiment 3 investigated whether prolonged T treatment or sexual experience could reverse the deficits in masculine behavior caused by the absence of T during puberty. Extending the T treatment from 7 to 17 days did not ameliorate the deficits in masculine behavior caused by absence of T during puberty. Similarly, when the level of sexual experience was increased from one to three tests, the deficits in masculine behavior persisted. These studies demonstrate that gonadal hormones during puberty further masculinize and defeminize neural circuits and behavioral responsiveness to steroid hormones in adulthood.