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After ejaculation, the male rat emits an ultrasonic (22-kHz.) vocalization. This sound is produced repeatedly until about three fourths of the postejaculatory interval has elapsed. In this study, the occurrence of the vocalization was described, and physiological and behavioral evidence was presented that the postejaculatory vocalization reflects an inhibitory state that underlies the postejaculatory refractory period. The vocalization period was characterized by a predominance of slow-wave, spindling, sleep-like electroencephalographic activity. Electrical shock was able to stimulate mating responses only after the cessation of the vocalization period. It was concluded that an absolute refractory period of the postejaculatory interval lasts until the end of the vocalization period and that the time from the termination of the vocalization until the resumption of mating is a relative refractory period.

ULTRASONIC vocalisations commonly occur during social interactions among rodents. During mating, adult male and female rats (Rattus norvegicus) emit brief 50-60 kHz ultrasonic calls1; however, the function of these vocalisations is not known. In this study, we demonstrate that these mating calls have a precise function for communication. Specifically, 50-kHz vocalisations elicit sexual activity in female rats. Female rats exhibit a series of solicitation patterns during sexual behaviour, including orientation, darting and ear wiggling. These movements excite the male and enhance the likelihood of mounting, thereby facilitating copulation2-4. (Beach has emphasised the importance of solicitation by the female during mating and has suggested the term 'proceptivity' to include the female's behaviour in the initiation and maintenance of copulation.) Although the presence of an intact male is usually a prerequisite for solicitation behaviour, the specific sensory cues which elicit it are not known. Isolated oestrous female rats exposed to ultrasonic vocalisations from a male exhibited a shorter latency to, and higher rate of darting when subsequently placed in a mating situation5. Although the auditory cues primed oestrous females to display increased solicitation behaviour when later confronted with an intact male, there was no indication that these ultrasonic vocalisations had a direct function for communication in the induction of these behaviour patterns. The objective of the present report was to determine if ultrasonic mating calls of rats have a direct function for communication during copulation. © 1978 Nature Publishing Group.

Solitary estrous female Long-Evans rats were presented with ultrasonic vocalizations and/or urine of males to determine their effects on the females' subsequent copulatory behavior. Following exposure to ultrasounds, females exhibited a shorter latency to dart and a higher rate of darting when a male was presented. The vocalization effect was enhanced when male urine was present, but urine alone had no effect. The rate of copulation was also increased by the vocalization priming of the female. For a few individual females, ultrasounds elicited darting in the absence of a male. Results indicate that auditory cues, particularly in association with appropriate olfactory cues, prime estrous females for proceptive behavior. This increases both the likelihood and the rate of sexual performance and, therefore, the probability of successful mating. (17 ref) (PsycINFO Database Record (c) 2006 APA, all rights reserved). © 1978 American Psychological Association.

During the refractory period that follows ejaculation, the male rat regularly emits 22-kilohertz vocalizations. These cease after about three-fourths of the total period has elapsed, and this corresponds to an "absolute refractory period" during which the male cannot spontaneously initiate copulation. Similar 22-kilohertz vocalizations occur in other social contexts, and in general they appear to be desist-contact signals.

Ultrasonic vocalizations were tape recorded from five pairs of copulating mice and subjected to spectrographic analysis. As expected, the mice emitted numerous 70-kHz vocalizations. At the beginning of the test, before copulation began, 70-kHz calls were emitted almost continuously, while calls with lower spectrographic frequencies were not observed. Subsequently, bursts of 70-kHz calling generally began shortly before mounts and intromissions and persisted until dismount. Intermixed with these 70-kHz calls were additional vocalizations of about 40 kHz. Calling rates were highest just prior to intromission. Once intromissions began, 70-kHz calls continued at a lower rate until dismount; however, 40-kHz calls occurred infrequently. In a second experiment, the male was found to emit the majority of the 70-kHz calls and all of the 40-kHz calls. When the male was devocalized, few calls were detected, regardless of whether the female was able to call. If the male was not devocalized, high rates of calling were detected, even if the female was devocalized.

Rat pups emit broadband vocalizations with components extending from the audible to the ultrasonic range. Three experiments were undertaken to determine the circumstances under which the calls are emitted, and the effects that they might have on the maternal female's behavior. In the first study, pups were manipulated by the experimenter in several different ways. Broadband calling occurred when the pup was picked up and moved off the horizontal plane. In a second study, the mother was observed interacting with her litter. Vocalizations occurred most often when the mother engaged in behaviors that brought her into contact with the pups, such as nest entry, moving while in the nest, and pup licking. In another experiment, females were temporarily deafened. Relative to controls, deafened females engaged in more incidental contact with the pups, although only if the female was deafened during the first of two tests, when the pups were two days old. Broadband calling may function to reduce rough handling or inadvertent contact by the mother.

Previous studies indicate that somatosensory inputs to the snout and the ventral trunk play critical roles in the elicitation and maintenance of maternal aggression by postpartum lactating Long-Evans Norway rats toward a strange male intruder. In the present studies we examined the possible influence of visual and auditory stimuli in the display of this behavior. In Experiment 1, dams temporarily deprived of visual or auditory input by eyelid suturing or ear molds, respectively, on Day 2 postpartum, were found to have normal levels of maternal aggression 1 day later. In Experiment 2, males were found to contribute about 50% of the short-duration 50-kHz vocalizations, which begin shortly after introduction of the intruder, and all of the long-duration 22-kHz vocalizations, which begin after the onset of attacks. Nonetheless, females tested with males surgically devocalized 7 days earlier were not significantly different in aggressiveness from dams tested with vocalizing males on either Day 1 or Day 4 postpartum. These findings indicate that visual or auditory inputs from the pups or intruder are not critical to the display of maternal aggression in rats, at least within the confines of laboratory housing.

Copulatory behavior and associated social behaviors such as ultrasonic vocalizations and scent marking are reduced in frequency following castration and are restored by exogenous administration of androgens. In the present study, we report the behavior of a subgroup of male Long-Evans rats in which there was a dissociation between the responses of androgen-dependent behaviors to castration. Five weeks after castration, 52% of the males tested (13 of 25) had higher 50 kHz vocalization frequencies than during precastration tests. This group continued to emit vocalizations after castration and actually increased their number of vocalizations over postcastration tests (pretest: 34.5 +/- 4.8 to week 15: 62.8 +/- 10.9/10 min test). The remaining males (n = 12) exhibited a decline in vocalizations (pretest: 29.7 +/- 5.1 to week 15: 6.5 +/- 2.7) that we typically observe in our laboratory. Both groups showed the expected decline in scent-marking frequency over the postcastration tests and were impaired in performance of copulatory behavior. Seminal vesicle and adrenal gland weights did not differ between the two groups. The 25 males were of the same genetic strain as previous animals in our laboratory except that they were born and raised in a different location prior to shipment to our laboratory. Androgens, therefore, may be only one of the possible influences mediating ultrasonic vocalizations.

Castrated male mice were bilaterally implanted with 27 ga cannulae containing testosterone into either the septum, medial preoptic area (MPO), or corticomedial amygdala. One additional group of castrates received no hormone and another received only systemic testosterone via subcutaneous silastic capsules. All males were subsequently tested for ultrasonic mating vocalizations, urine marking, mounting behavior, aggression and gender preference, all of which are androgen-dependent, male-typical behaviors. In general castrates receiving no hormone performed these behaviors at low levels and animals receiving systemic testosterone performed the behaviors at normal male-typical levels. Ultrasonic vocalizations in response to female urine were activated by MPO implants. Urine marking in response to female urine appeared to be partially activated only with MPO implants. Very little mounting or fighting were seen in the brain implanted groups. Gender preference (for females over males) was restored with MPO implants and appeared to be partially activated with septal implants. The seminal vesicles of the castrates receiving brain implants were not significantly different from those receiving no hormone indicating that little or no implanted hormone was exiting the brain into general circulation. The implications of these findings for the neuroanatomy of sexual motivation and performance are discussed.

RU 486 is known primarily as an antagonist to progestins and glucocorticoids. However, RU 486 has also been shown to have agonistic progestational properties in biochemical and behavioral studies. In the current study, RU 486 was implanted directly into the ventromedial hypothalamus (VMH) to test for facilitative action on the receptive behavior of female ovariectomized Long-Evans rats primed with 5 micrograms of estradiol benzoate. Cannulae containing RU 486, progesterone (P), or empty cannulae were implanted 48 hr after estrogen priming. The lordosis quotient and the lordosis score were assessed 4 hr after the cannulae were lowered by a standardized test consisting of 10 mounts by a stimulus male. P and RU 486 significantly facilitated receptivity compared to blank implants in terms of lordosis quotient and lordosis score, with no significant difference between the hormone treatments. While only a single dose of each treatment was given in the current study, RU 486 facilitated lordosis when implanted to the VMH as well as progesterone in contrast to our previous results where the steroids were administered systemically.

Female rats emit calls during copulation that appear to be associated with their own proceptive behavior. In an earlier study, we had determined that females emit calls when presented with odor cues from a sexually competent adult male. Two experiments were undertaken to determine whether females would vocalize when presented with tape recorded male ultrasonic vocalizations. In the first females were presented with no calls, male mating calls or male preejaculatory calls. They received one test in each sound condition with a devocalized male in the immediate vicinity and one test with no male present. Females tested alone called at a lower level than those tested in the presence of a devocalized male. The presence of male calls did not significantly increase the frequency of calling in females tested in the presence of a male. When females were tested alone, however, calling did increase significantly when male mating calls were presented, but not when preejaculatory calls were presented. In a second experiment, it was confirmed that male mating vocalizations elicited more calls from the female. Thus, male mating calls may elicit vocalizations from the female, but are less effective than male odor cues.

Two experiments examined the role of the steroid hormones, estradiol (E2), progesterone (P), and testosterone (T), in activating scent marking and 50-kHz ultrasonic vocalizations in ovariectomized Long-Evans rats in response to a devocalized male rat. In Experiment 1, females received, in a counterbalanced order, a series of six hormone treatments consisting of two injections (48-54 and 4 hr before behavioral tests). The six treatments were 8 micrograms E2 followed by 500 micrograms P or oil, 2 micrograms E2 followed by 500 micrograms P or oil, and oil followed by 500 micrograms P or oil. Injections of either the high or low dose of E2 followed by P resulted in high levels of vocalizations. Neither E2 by itself or P by itself were very effective. Surprisingly, none of the hormone treatments were effective in activating marking above the level seen when the females received control injections of oil. Four other hormone treatments were examined in Experiment 2: daily injections of 500 micrograms T, daily injections of 50 micrograms E2, implantation of silastic capsules of E2 (5% E2, 5 mm length) followed by 500-micrograms P injections before behavioral tests, and implantation of silastic capsules of E2 followed by oil injections. Animals receiving E2 by silastic capsule followed by P injection displayed the highest levels of marking and vocalizations across the five weekly tests. These results suggest that while E2 and P synergize for the display of female-typical behaviors similar to the hormonal regulation of lordosis, the mechanism of E2 action may be different for the two signaling behaviors. Scent marking appears to be responsive to the tonic levels of E2 released from silastic capsules.

Pups emit a broadband vocalization ranging from 2 to 40 kHz that generally occurs when the mother sits or steps on her pups. In an earlier study (Ihnat, White, and Barfield, under review), we noted that the mother was more likely to move on the pups and step on them when she was temporarily deafened with ear plugs. This research was extended in the present study by using two different methods to prevent 2-day-old pups from emitting broadband vocalizations. In the first experiment, the female was presented with six of her pups for a 10-min test. In half the tests, the pups had been anesthetized with pentobarbital; in the other half, the pups received saline. In the second experiment, females were presented with pups whose mouths had been sealed with an adhesive substance. In a final study, pups received the adhesive substance on their ventral surface as a control. When the pups were unable to vocalize, there was an increase in the amount of time per bout that the mother spent in incidental contact with her pups; in the sham condition, however, there was no change in her behavior. In addition, the female was less likely to group all her pups within the 10-min duration of the test when the pups could not call. Since pups emit primarily broadband vocalizations in response to handling prior to 4 days of age, broadband calls appear to reduce incidental contact and facilitate retrieval into a group.

The purpose of the present study was to investigate whether the signaling behaviors of female Long-Evans rats varies over the estrous cycle. Scent marking and 50-kHz ultrasonic mating vocalizations, in response to a devocalized sexually experienced male, changed in frequency across the cycle, both behaviors being highest at proestrus/early estrus. Vocalizations were recorded on every day of the cycle and also in females showing no regular cycles. In contrast, scent marking was rarely observed during the estrous cycle except at proestrus/early estrus. These results suggest that both behaviors, which increase around the time of sexual receptivity, may help to coordinate reproduction and further suggest an endocrine basis for the changes observed over the estrous cycle.

Two experiments in house mice (Mus domesticus) examined the neural sites at which steroid hormones activate the following male-typical behaviors: 70 kHz ultrasonic mating vocalizations in response to stimulus females or their urine, urinary marking in response to stimulus males or stimulus females, mounting of estrous females, and intermale aggression. In the first experiment, four groups of castrated males received bilateral intracranial implants of testosterone (T) into either the septum (SEPTUM), medial preoptic area (MPO), anterior hypothalamus (AHA), or ventromedial hypothalamus (VMH). Two control groups received subcutaneous silastic capsules of T (TSIL) or empty silastic capsules (BSIL). The TSIL males performed all behaviors at male-typical levels while the BSIL males were unresponsive. MPO males emitted ultrasonic mating vocalizations at high levels while few vocalizations were seen in males of the other brain implant groups. The VMH, AHA, and MPO males urine marked at higher levels than the BSIL males but did not exhibit the high levels of the TSIL males. Mounting was observed only in MPO and TSIL males. Aggression was rare in males from any of the brain implant groups. In the second experiment, the hormone activity of the implants was increased by using testosterone propionate (TP) or a 50% mixture of estradiol (E2) and cholesterol. The six groups were SEPTUMTP, SEPTUME2, MPOTP, MPOE2, TPSIL, and BSIL. The TPSIL males performed all behaviors at male-typical levels while the BSIL males were unresponsive. TP was effective at restoring vocalizations and urine marking only when placed in the MPO; however, E2 was effective at both sites. Again aggression and mounting were less evident in the brain implanted males. In conclusion, implants of T or TP were effective in restoring ultrasonic mating vocalization when placed into the MPO. MPO implants of T and TP were also effective in stimulating urine marking, although VMH and AHA implants also showed some effectiveness. The restorative effects of E2 were not localized which is probably related to the greater hormonal activity of this treatment. Comparisons of the properties of the various brain implants to restore more than one behavior were discussed.

RU 38486 (RU 486, mifepristone) is a potent progesterone receptor antagonist that has been used in humans in the pharmacologic induction of abortion. The effects of exposure to RU 486 during the neonatal period of the rat has not been previously reported. We examined the consequences of such exposure in the context of sexual development. Long-Evans rat pups were subcutaneously injected with either 100 micrograms RU 486, 300 micrograms RU 486, 500 micrograms progesterone (P), or 50 micrograms testosterone propionate (TP) in 0.05 ml sesame oil, or oil vehicle alone within 8 hours of birth, and 24 and 48 hours later. Treatment with either dose of RU 486 significantly advanced the onset of vaginal opening in females and attenuated defeminization of the lordosis response measured in males castrated as adults. As expected, TP-treated subjects were masculinized and defeminized, with females displaying fused vaginas and neither males nor females demonstrating lordosis behavior. Treatment with P caused no significant alterations in either the timing of vaginal opening or sexual behavior. These results indicate that RU 486 has clear developmental effects in the rat. Since this may well be a result of progesterone receptor blockade, further research is needed to clarify the processes involved.

The effects of testosterone (T) and its major metabolites, estradiol (E2) and dihydrotestosterone (DHT), on the restoration of sebaceous scent marking and 50-kHz ultrasonic vocalizations in male rats were measured in two studies (Experiments 1 and 2) employing different hormone levels. Silastic capsule administration of high and low doses of T (10 and 20 mm) or E2 (5%; 5 and 10 mm) completely restored marking to precastration levels. Both doses of DHT (30 and 40 mm) or no hormone replacement were without effect when tested in presence of estrous odor cues. In our testing paradigm, males appeared to mark glass objects with a sebaceous secretion rather than urine. Only the high dose of T (20 mm) restored vocalizations to intact levels, while animals receiving the high or low dose of E2 or DHT showed no restoration of behavior. In Experiment 3, habituation to estrous odor cues over weekly tests was not observed for marking or vocalizations. These results are discussed with respect to similarities and differences in the hormonal control of signaling behaviors by androgen metabolites in male rodents.

Progesterone (P) facilitation of sexual receptivity in rodents has been achieved by intracranial administration to the ventral hypothalamus; the preoptic area; and midbrain areas such as central gray, mesencephalic reticular formation, and ventral tegmental nucleus. In our laboratory, by far the most effective site in rats has been the ventromedial nucleus of the hypothalamus (VMN). However, several reports of sensitivity to P in the midbrain of rats and other rodent species led us to investigate whether stimulation of the ventral midbrain of female rats might contribute to facilitation of sexual receptivity. Ovariectomized Long-Evans rats received one cannula aimed at the VMN, and another aimed at the contralateral ventral mesencephalon. P in both cannulae, following a priming dose of estradiol, caused significantly higher lordosis quotients (LQ) than blank tubes. Controls with bilateral cannulae in the VMN responded when both tubes were filled with P, but did not respond to unilateral VMN P stimulation. P in the VMN and contralateral anterior preoptic area did not result in a greater degree of receptivity than did the empty tubes. These studies indicate that although progesterone stimulation in the midbrain alone is not sufficient to facilitate receptivity in female rats with our methods, the midbrain may play an auxiliary role. P implants in the midbrain appear to facilitate receptivity in the case of VMN implant treatments that are subthreshold for stimulating lordosis. The results are discussed in light of similar studies in other rodent species, and in the context that more than one brain site may be important in the natural stimulation of sexual receptivity by gonadal hormones.

Female rats emit ultrasonic vocalizations during copulation. Female vocalizations are associated with darting and other proceptive behavior. In addition, females frequently call while approaching the male. A series of experiments was undertaken to determine whether female rats emit ultrasonic vocalizations in response to other rats or to their odors. Females were exposed either to bedding soiled by males or females or to devocalized conspecifics separated from the subject by a barrier. Females vocalized more to male cues than to female cues, regardless of whether the odor cues were from soiled bedding or from a devocalized conspecific. In addition, subjects vocalized more when presented with a devocalized female rather than a neutral stimulus. Furthermore, devocalized adult males, separated by a barrier, were more effective than either devocalized castrated or juvenile males in eliciting vocalizations; in turn, castrates and juveniles were more effective than neutral stimuli. Female calling was likely induced by odors from the male. In one experiment, the female subject was positioned in such a way that she could neither see or touch the stimulus male. Presentation of tape-recorded male vocalizations did not affect calling by the female. Vocalizations emitted by females in response to male odors may attract males or may facilitate subsequent copulatory behavior by the male.

Rats (Rattus norvegicus) produce ultrasonic calls during mating. We examined changes in the structure and pattern of such vocalizations over the ejaculatory series. In Experiment 1, vocalizations were recorded from 11 pairs of rats through 3 ejaculatory series and analyzed spectrographically. We classified 4 categories of call by spectral frequency and duration. Calls of low frequency, long duration, and high intensity occurred more often shortly before the ejaculation and were associated with mounting without intromission, a behavior that often occurs shortly before ejaculation. The high-frequency calls did not vary in number across the series. In Experiment 2, vocalizations were recorded from males paired with devocalized females. Males produced all vocalization patterns produced by pairs in Experiment 1. Results suggest that most pre-ejaculatory calls are produced by males and may potentially affect female sexual behavior.

The progestin receptor antagonist RU 38486 (henceforth referred to as RU 486) was tested for facilitative effects on female receptive behavior in ovariectomized Long-Evans rats primed with 2 micrograms estradiol benzoate (EB). RU 486 (0, 0.5, 1.6, or 5.0 mg) was administered 48 hr after estrogen priming. The lordosis quotient (LQ) and lordosis score (LS) were assessed 4 hr after RU 486 administration in a standardized test consisting of a 10-mount test by a stimulus male. A significant dose effect was found by both LQ and LS, with those subjects receiving 5 mg of RU 486 being significantly more receptive than vehicle control animals. Thus RU 486 acted as a weak progestin agonist under testing conditions typical for assessment of progestin facilitation of female sexual behavior in rats. Low levels of proceptive behavior (hops and darts) were seen in a minority of the tests, and did not vary systematically as a function of the dose of RU 486 administered. We also examined the effects of RU 486 given before progesterone (P) on receptivity in a blocking paradigm and confirmed previous reports that the antagonist significantly attenuates facilitation of sexual behavior when given in combination with P. A progestin receptor assay of the cytosols of the hypothalamus-preoptic area in estrogen-primed female rats treated with 5 mg RU 486 revealed a significantly greater depletion of available cytosolic P receptors than when rats were treated with a similarly facilitating dose of P (100 micrograms). The results suggest a possible dual mode of action for RU 486--a weak, receptor-mediated agonistic effect on sexual behavior when given alone to estrogen-primed rats, and a competitive blocking effect on receptivity when administered with P.

Extracellular dopamine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC) in the nucleus accumbens (N. Acc.) were measured by in vivo microdialysis during male sexual activity. DA and DOPAC were significantly increased during copulation, but not during mild tail pinch. These results are consistent with studies showing increases in N. Acc. DA associated with positively reinforcing environmental stimuli.

Both male and female rats (Rattus norvegicus) emit ultrasounds during copulation. Bursts of ultrasounds from males that occur as ejaculation approaches are lower in frequency, longer in duration, and louder than those that appear earlier in the ejaculatory series. We attempted to determine if these pre-ejaculatory calls affect female sexual behavior. The behavior of females paired with devocalized males was compared with that of females paired with intact males, and in a second experiment tape-recorded vocalizations were played to females paired with devocalized males. Females were less receptive when paired with devocalized males; they were less likely to remain stationary when males attempted to mount. Playback of both types of calls restored female immobility toward control levels, although pre-ejaculatory calls were more effective than mating ones. Pre-ejaculatory calls restored running and training levels somewhat toward control level but to a lesser extent than female immobility.

Male rats (Rattus norvegicus) emit at least two patterns of vocalization during copulation, the mating call and the pre-ejaculatory call. Both calls promote immobility of the female during lordosis, but the pre-ejaculatory calls are more effective. We undertook, through ventral observations of the mating pair, to determine if the female failed to assume or maintain the lordosis posture when mounted by a devocalized male and also to determine if the devocalized male was providing adequate stimulation to induce receptive behavior. Females were more likely to move away from the devocalized males before assuming the full lordosis posture. Furthermore, they were more likely to move away before the males had a chance to engage in intromissive behavior. However, when the females remained immobile long enough for the males to achieve a mount or intromission, there was little difference in the behavior of either animal that resulted from the devocalization of the male.

Cells in the male fowl brain which accumulate radioactivity following 3H testosterone (T) administration were identified by autoradiography. Labelled cells were found principally in hypothalamic, limbic and midbrain structures. Marked uptake was observed in the preoptic area (POA) and in the anterior and posterior hypothalamus. There was also a significant amount of labelling in the archistriatum (ARCH), particularly in the nucleus taeniae (Tn), and in the lateral septum. In the midbrain, substantial uptake of labelled hormone was found in the nucleus intercollicularis (ICo). The pattern of accumulation of T in the male fowl was comparable to that for sex hormone uptake in vertebrates in general. Furthermore, accumulation was generally found in areas known to be concerned with sex hormone-dependent functions.

The present study was carried out in order to assess the time course of action of progesterone (P) in the facilitation of complete feminine sexual behavior. Female rats (estrogen primed via 5% E2 Silastic capsules) were given 200 micrograms of P either intravenously (iv) or subcutaneously (sc), and tested for estrous behavior at 1/4, 1/2, 1, 2, and 4 hr after treatment. Among iv-treated animals, significant amounts of lordosis behavior were seen as early as 1/2 hr, and a dramatic rise in solicitation behavior was observed at 2 hr. Although sc-treated animals displayed significant amounts of lordosis and solicitation behavior at 2 hr, the behavior was not maximal until 4 hr. Intravenous administration of 400 micrograms P was equipotent to 200 micrograms P, whereas 50 micrograms of iv P was relatively ineffective. A dual mechanism hypothesis pertaining to progesterone's actions in the facilitation of both the receptive and proceptive components of feminine sexual behavior in rats is discussed.

This study was designed to examine the role of central dopaminergic mechanisms in the control of copulation and the subsequent post-ejaculatory refractory period in the male rat. Disruption of central dopaminergic pathways was achieved in two separate groups of animals by: (1) selective electrolytic lesions of the substantia nigra (the major locus for dopamine cell bodies in the brain); or (2) localized intracerebral injection of 6-hydroxydopamine, a specific neurotoxin for catecholaminergic pathways. A third group of animals was tested for sexual behavior following administration of the dopamine receptor blocker pimozide. Both electrolytic and neurochemical lesions localized in the substantia nigra produced a significant increase in the length of the post-ejaculatory refractory period. Dopamine receptor blockade following administration of pimozide also caused a significant increase in refractory period duration. These results support the hypothesis that central dopaminergic pathways are involved in the motivational or arousal component of copulation and may be integral to the maintenance of a normal post-ejaculatory refractory period.

This investigation was concerned with the identification of the ultrasonic vocalizations produced by intruders during aggressive interactions and the role of these signals in agonistic behavior of rats. In the first experiment, experienced resident males were paired with both devocalized and intact vocalizing naive intruder males. Devocalization of the intruder males resulted in a drastic decrease in 50-kHz vocalizations and the elimination of all 22-kHz vocalizations. This almost total absence of ultrasonic vocalizations was not accompanied by any change in resident aggressive behavior or intruder defensive and submissive behavior. In a second experiment, naive intruders were tested with either deafened or intact resident males. Similarly, preventing residents from hearing intruder ultrasounds had no detectable effect on any aggressive behavior. These experiments are not consistent with the correlative evidence that intruder-produced 22-kHz vocalizations inhibit the aggressive behavior of the resident. The results also show that most of the ultrasonic vocalizations emitted during aggressive encounters are probably produced by the intruder.

The present experiment was performed to examine the role of serotonergic mechanisms in the control of copulation and the post-ejaculatory refractory period in the male rat. Disruption of central serotonergic systems in two separate groups of animals was achieved by: (1) selective electrolytic lesions of the midbrain raphe nuclei, or (2) localized intraventricular or intracerebral injection of a specific serotonergic neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT). A third group of animals was tested for sexual behavior following intraperitoneal injection of p-chlorophenylalanine (PCPA), an inhibitor of serotonin synthesis. Both electrolytic and neurochemical lesions localized in the dorsal raphe nucleus produced a highly significant shortening of the ejaculatory latency, and the post-ejaculatory refractory period. Disruption of serotonergic mechanisms following intraventricular injection of 5,7-DHT or systemic administration of PCPA also caused a significant reduction in the length of the refractory period. These results support the hypothesis that central serotonergic systems are normally inhibitory to certain facets of male copulatory behavior and suggest the existence of a serotonergic control system which normally exerts an inhibitory influence over the resumption of mating following ejaculation.

The CNS sites of action for progesterone facilitation of female sexual behavior are disputed. Among the areas most often cited are the ventromedial hypothalamus and the ventral midbrain. There is also a controversy about whether estradiol may substitute for progesterone for the facilitation of receptive behavior when given systemically or intracranially. We tested VMH and ventral midbrain applications of estradiol versus progesterone for the facilitation of female sexual behavior in estrogen-primed, ovariectomized female rats. Subjects were implanted with bilateral guide tubes aimed at ventral hypothalamic or midbrain sites. Estrogen-primed rats received either 28-gauge insert cannulae filled at the lumen with pure progesterone, estradiol, or cholesterol, or empty tubes, and were tested for receptivity with intact, experienced stud males just before, and 1 and 4 hr after, intracranial hormone administration. Significant estrous responsiveness was seen only in the 4-hr test after progesterone was implanted in the VMN in the first intracranial cannula test. We conclude, in contrast to some previous reports, that administration of progesterone to the VMN is more effective in the facilitation of female sexual behavior than when it is implanted in the ventral midbrain, and that administration of estradiol to either site is ineffective.

For the purpose of testing the hypothesis that the high level of aggressive behavior exhibited by postparturient rats is mediated by lactogenic hormones, hypophysectomy was performed on Day 5 postpartum, and fighting against an adult male rat was measured 4 days later. Pups were exchanged daily between hypophysectomized and sham-operated or unoperated controls animals. In Experiment 1, no differences in aggressive behavior were seen between hypophysectomized, sham-hypophysectomized, and untreated lactating animals on Day 9 postpartum. In Experiment 2, the hormonal dependence of the characteristic sensitivity to the presence of the litter in the elicitation of postpartum aggression was investigated. All animals were tested three times, on Day 9, 12, and 15 postpartum; litters were removed 4 hr prior to the second aggression test. For all groups, aggression levels were high on Day 9 with the litter present, dropped on Day 12 after removal of the litter, and showed some increment or stabilization on Day 15 with the litter again present. These experiments demonstrate that neither the expression of postpartum aggression nor the sensitivity to the presence of stimuli from the litter is directly dependent upon the hormonal milieu characteristic of lactation.

The present experiment was designed to determine whether sequential replacement of estrogen and progesterone to the ventromedial hypothalamus (VMH) would be sufficient to induce estrous behavior in ovariectomized rats. Bilateral cannulae containing 17 beta-estradiol (E2) diluted with cholesterol (1:250) were lowered into the VMH, preoptic area or midbrain and left in place for 4 days. On day 5, the E2 inserts were removed and P-filled cannulae were lowered into half of the subjects. The remaining females received systemic progesterone (500 micrograms). This steroid regimen was repeated 2 weeks later with the mode of progesterone administration reversed. All subjects were tested for estrous behavior twice after progesterone treatment. In a second experiment, 3H-P:P-filled cannulae were lowered into the VMH of estrogen-primed females in order to estimate the extent of hormone spread from full-strength P-filled cannulae. Results indicated that estrogen and progesterone stimulation of the VMH is sufficient to activate estrous behavior in spayed female rats, however, precise localization of the hormone implants within the VMH is essential. 9 of the 11 females with both cannulae located within or at the border of the ventromedial nucleus (VMN) exhibited estrous behavior whereas only half of the females with only one implant resting in the VMN exhibited estrous responsiveness. Subjects with neither cannula located within or at the border of the VMN did not exhibit the behavior. The facilitative effects of P appeared to result from hormonal stimulation of the VMH and not from leakage of the steroid into other brain regions or into the systemic circulation. Following placement of tritiated progesterone implants into the VMH, high levels of radioactivity were recovered only from the mediobasal hypothalamus. The low levels of radioactivity measured in other brain regions, pituitary, uterus and blood indicate that relatively little if any hormone reached these tissues.

In this article we review research on the role of progestins in the regulation of estrous responsiveness in female rats. Estrous responsiveness normally results from a synergistic action of estradiol (E2) and progesterone (P). E2 primes the system but normally does not result in estrous behavior. The full expression of estrous responsiveness results from the action of P on the E2-primed system. It has been demonstrated with implants of dilute E2 (1 part E2: 250 parts cholesterol) that the site of E2 priming is the ventromedial nucleus of the hypothalamus (VMN). In females primed with systemically administered E2, P also acts on the VMN to facilitate full estrous responsiveness. It has been shown in addition that estrous responsiveness results from sequential application of E2 and P to the VMN but not to other areas of the brain. The VMN is also the site at which P produces sequential inhibition of estrous responsiveness. The time course of P action in facilitating full estrous responsiveness is about two hours, regardless of whether the hormone is administered intracerebrally or intravenously. The duration of estrous responsiveness is directly correlated with the length of time P is in contact with brain tissue. Experiments with the protein synthesis inhibitor anisomycin are consistent with the view that P acts in the VMN by way of a protein synthetic mechanism to facilitate estrous behavior; however, other mechanisms must be considered as alternatives. Finally, we address the question of whether estrogenic priming depends upon induction of progestin receptors in the VMN. Results indicate that estrogenic priming of estrous responsiveness may occur without concomitant induction of progestin receptors.

The hypothesis that progesterone (P) activates estrous behavior in estrogen-primed female rats via a protein synthetic mechanism was examined. The protein synthesis inhibitor anisomycin was applied intracerebrally via 28-gauge bilateral implants to neural sites implicated in the mediation of estrous responsiveness. Results showed that anisomycin blockade of P-activated estrous behavior was neural site specific. Animals with anisomycin placed in the ventromedial hypothalamus (VMH) (n = 27) showed low levels of lordosis and solicitation behavior 4 h after the subcutaneous administration of 500 micrograms P, whereas animals with anisomycin implants in the preoptic area (n = 11) or the midbrain area in the region of the interpeduncular nucleus (n = 11) displayed high levels of estrous behavior. No deficits in open-field activity were observed following localized anisomycin treatment, and all animals appeared to be healthy. Results of the present study are consistent with the hypothesis that P acts to promote estrous behavior via a receptor-mediated genomic protein synthetic mechanism, and provide additional evidence that the VMH is the primary site of P action.

Ultrasonic vocalizations were measured when male rats were placed with ovariectomized females that had experienced various hormonal and behavioral treatments. In Experiment 1, 18 males were tested with females in each of the following conditions: nonestrous (OVX), estrogen treated (E), estrogen and progesterone treated (EP), and estrogen and progesterone treated and given two intromissions from a stud male prior to testing (EPI). Control conditions included clean cage (CL) and cage soiled by an estrous female (SOI). The treatments differed in effect on rate and maintenance of vocalization: EP greater than E greater than EPI = OVX greater than SOI greater than CL. In tests in which males produced a high rate of vocalization, some males with short intromission latencies shifted from the normal 50-kHz pulse to a 22-kHz pulse. In Experiment 2, the effect of the female's vocalization and movement on the rate of and latency to vocalization was measured. Twenty-one males were presented with each of the following stimulus conditions: estrous female with red light (EP), estrous female without red light (EP dark), estrous anesthetized female (EP anes), and nonestrous anesthetized female (OVX anes). Effects on vocalization of various treatments were as follows: EP = EP dark greater than EP anes greater than OVX anes. These data suggest that the 50-kHz vocalizations constitute a graded response influenced by the female's hormonal and sexual condition.

To investigate whether metabolism of progesterone (P) to other progestins is necessary for the facilitation of estrous behavior in estrogen-primed rats, we evaluated the behavioral effectiveness of intrahypothalamic implants of two P metabolites, 5 alpha-dihydroprogesterone (DHP) and 20 alpha-hydroxyprogesterone (20HP), and of desoxycorticosterone (DOC). We also determined whether the progestin receptor binding capacity of the steroids correlated with their behavioral efficacy. Implants of DHP and 20HP into the ventromedial hypothalamus were considerably less effective than P in activating estrous behavior; in contrast, the mineralocorticoid DOC was nearly as effective as P. Binding studies showed that P had the highest affinity for brain progestin receptors followed by DHP, DOC and 20HP. Thus there was a poor correlation between the behavioral efficacy and the progestin receptor binding properties of the steroids tested. These data suggest (1) that neither 5 alpha-reduction nor 20 alpha-hydroxylation are necessary for P activation of estrous responsiveness and (2) that the structural features required for the behavior promoting effects of P may not be identical to those required for binding to brain progestin receptors.