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R J Barfield

Publications and source records attributed to R J Barfield.

At least 37 records · Page 2Linked to original sources
PubMed1990

Changes in mating vocalizations over the ejaculatory series in rats (Rattus norvegicus).

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.

Animals↗
PubMed1989

Actions of RU 38486 on progesterone facilitation and sequential inhibition of rat estrous behavior: correlation with neural progestin receptor levels.

The present study examined the actions of the antiprogestin RU 38486 on progesterone (P)-induced facilitation and sequential inhibition of estrous behavior and on brain cytosol progestin receptor (PR) levels in ovariectomized, estrogen-primed (0.5 micrograms of estradiol benzoate for 3 days) female rats. RU 38486 suppressed P-facilitated receptive and proceptive responses in a dose-dependent fashion when administered 1 hr prior to P. RU 38486 did not, however, block the sequential inhibitory effect of P. Indeed, when it was administered alone at a dose of 1 mg, animals were rendered behaviorally unresponsive to a P treatment 25 hr later. It is unclear whether RU 38486 is an agonist for P sequential inhibition of estrous behavior or if the apparent agonist action of RU 38486 actually results from a long-term antagonist effect. Estrogen-induced PRs remain elevated (35-55% above basal) in the hypothalamus (HYP) and preoptic area (POA) at 24 and 48 hr following the last estrogen injection. Thus P facilitation of estrous behavior is correlated with increased levels of cytosol PRs. RU 38486 reduced cytosol PRs in both brain regions to basal levels within 2 hr, and the levels remained suppressed 25 hr following the treatment. Hence there is a strong correlation between behavioral inhibition and suppressed cytosol PRs at both short (5 hr) and long (25 hr) intervals after RU 38486 administration. A P treatment which produced sequential inhibition of estrous responsiveness 24 hr later did not reduce the estrogen-induced level of cytosol PRs in either brain region. These results suggest that mechanisms in addition to induction of PRs may be necessary to ensure successful mating.

Animals↗
PubMed1989

Playback of female rat ultrasonic vocalizations during sexual behavior.

Both male and female rats emit ultrasonic vocalizations during mating. In an earlier study, female vocalizations were shown to be associated with female darting: when the female was devocalized, she increased her rate of darting. In a preliminary playback study, tape-recorded female ultrasounds were presented to devocalized females paired with intact males. Darting was reduced towards presurgical control levels. In this study, the playback experiment was replicated using a refined procedure to present female ultrasounds to the mating rats. Taped vocalizations were obtained from females, and were presented in a manner which more closely approximated the patterning of ultrasound production seen in the intact female. Each rat pair was tested three times: once prior to the devocalization of the female, and twice afterwards. In one postsurgical test, taped ultrasounds were presented during mating; in the other, tape hiss was presented. Several patterns of behavior increased in frequency when the female was devocalized relative to the control condition, but decreased when tape recorded ultrasounds were presented. These patterns included female darting and approaches towards the partner by both males and females. The darting results confirm and extend the findings of our earlier paper. Changes in approach behavior were not observed previously because the male was confined in the earlier study. This study contains the first direct evidence that female vocalizations affect the socio-sexual behavior of the male.

Animals↗
PubMed1989

Mediation of rat postejaculatory 22 kHz ultrasonic vocalization by dopamine D2 receptors.

We investigated the role of dopamine receptor subtypes in the regulation of ultrasonic vocalization and masculine copulatory behavior. Intact sexually experienced male Long-Evans rats were treated with saline, selective dopamine D1 (SKF 38393) and D2 (LY 171555) receptor agonists and with selective dopamine D1 (SCH 23390) and D2 (raclopride) receptor antagonists 15 and 30 min before the 30-min test session, respectively. Mating stimuli were ovariectomized female rats injected SC with estradiol benzoate (8 micrograms/0.1 ml/rat) and progesterone (200 micrograms/0.1 ml/rat), 48 and 4 hr before the test session, respectively. We found a decrease in the number of intromissions required to reach ejaculation in animals treated with SKF 38393 (10 mg/kg/IP), LY 171555 (doses ranging from 0.01 to 0.5 mg/kg/SC) and with raclopride (0.1 mg/kg/SC). LY 171555 reduced the postejaculatory vocalization (PEV) in a dose-dependent fashion with complete suppression at the highest dose. No other parameters of sexual behavior were affected by this treatment. Raclopride, a dopamine D2 receptor antagonist, antagonized the suppressive effects of the D2 agonist LY 171555 on the PEV (and also decreased the number of intromissions to reach ejaculation), whereas SCH 23390, a dopamine D1 receptor antagonist, did not. Raclopride, given alone at the dose of 0.5 mg/kg/SC, almost completely suppressed all behavioral activity, whereas the lower dose (0.1 mg/kg) decreased intromission frequency and increased the length of the 22 kHz PEV. Therefore, we suggest that 22 kHz PEV is under the control of dopamine D2 receptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1989

Dilute estradiol implants and progestin receptor induction in the ventromedial nucleus of the hypothalamus: correlation with receptive behavior in female rats.

The ventromedial nucleus of the hypothalamus (VMN) is thought to constitute an essential neural substrate for hormonal induction of female sexual behavior. In previous work, implants of dilute (0.4%) estradiol (E2) have been found to prime progesterone-facilitated female sexual behavior in rats only when they are within or very close to the VMN. In other studies, induction of cytosolic progestin receptors (PRc) in the hypothalamus has been correlated with systemic E2 priming of receptive behavior. We combined dilute E2 implants with a Palkovits punch microassay for PRc in the an effort to examine the relationship between estrous behavior and estrogen-induced PRc in the VMN of individual female rats. Ovariectomized rats were given bilateral guide cannulae aimed at the VMN and were primed for 3 days with 1) blank implants plus oil sc, 2) blank implants plus 0.5 micrograms E2 benzoate sc, 3) implants of 0.4% E2 in cholesterol, or 4) implants of 2.0% E2. On day 4 all rats received progesterone (P) sc and were tested for receptive behavior. The following week all subjects received the same estrogen-priming treatment but were killed on day 4 without P treatment. The VMN was punch dissected and assayed for PRc. High levels of lordosis were seen in the E2 benzoate-treated and 2.0% E2-implanted animals, while little behavior was seen in the oil-treated animals. Among 0.4% E2-implanted animals, higher levels of lordosis were observed in subjects with implant placements in the rostral than in the caudal VMN; however, lordosis quotients were not correlated with PRc induction measured in the entire VMN of individual animals. In general, our findings suggest that local estrogenic stimulation of target cells in the VMN is capable of both priming the estrous response and induction of P receptors. Whether these two effects are causally related awaits future study.

Animals↗
PubMed1988

Subtle behavioural changes produced in rat pups by in utero exposure to haloperidol.

Prenatal exposure to a dopamine receptor blocking agent such as haloperidol (given to the mother at a dose of 0.5 mg/kg s.c. from day 4 to day 15 of gestation) produced subtle behavioural changes in rat pups. Haloperidol decreased the rate of ultrasonic vocalization in 4-day-old male pups removed from the nest. The changes in ultrasonic emission elicited by in utero exposure to this neuroleptic were markedly different from those produced by its administration during the early postnatal period. Moreover, adult male rats treated prenatally with haloperidol exhibited a significant increase in the intensity of ultrasonic 22 kHz post-ejaculatory calls emitted during sexual behaviour. The duration of the period of the 22 kHz calls emission was also significantly increased by haloperidol treatment. These results confirm that ultrasonic vocalization in rats is a sensitive indicator of subtle changes in adverse treatments administered during development.

Animals↗
PubMed1988

Progesterone versus estrogen facilitation of female sexual behavior by intracranial administration to female rats.

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.

Animals↗
PubMed1987

Actions of progestins on estrous behaviour in female rats.

The present study evaluated the facilitative actions of progesterone and the synthetic progestin R 5020 on estrous responsiveness in ovariectomized, estrogen-primed female rats. The dose-response and time-response characteristics of the behavior facilitating actions of both progesterone and R 5020 were measured. The threshold doses for the facilitation of estrous behavior in estrogen-primed female rats were 1 microgram of R 5020 and 100 micrograms of progesterone. These doses of progestins facilitated estrous responsiveness with a similar time course that approached maximum at one hour. To examine the possible mechanism(s) of action of each progestin the synthetic progestin antagonist RU 38486 was used. The inhibitory effects of RU 38486 on estrous behavior facilitated by a threshold dose of progesterone or R 5020 were found to be almost identical. RU 38486 (5 mg) administered 1 hr prior to progesterone or R 5020 suppressed lordosis behavior by 44% and 47% respectively. These results suggest that progesterone and R 5020 facilitate estrous responsiveness through the same mechanism.

Animals↗
PubMed1987

Temporal aspects of ventromedial hypothalamic progesterone action in the facilitation of estrous behavior in the female rat.

Progesterone (P) action following estrogen priming is required normally for the facilitation of estrous behavior in female rats. Although mechanisms by which P exerts its influence on estrous responsiveness have not been elucidated, the primary site of action of P has been shown to be the ventromedial nucleus of the hypothalamus (VMN). The objective of the present series of experiments was to describe the temporal parameters of P action in the VMN in the facilitation of estrous behavior in estrogen-primed female rats. Subjects were female Long-Evans rats stereotaxically outfitted with 23-ga. guide cannulae directed towards the VMN. Crystalline P was applied directly to the brain tissue via bilateral 28-ga. insert cannulae, which could be inserted and removed easily through the guide cannulae. Animals were ovariectomized and estrogen primed with 5% estradiol Silastic capsules. They received a counterbalanced series of two experimental tests: one involving a manipulation with a P-filled implant, and another with a blank implant. In the first experiment, a significant increase in estrous responsiveness occurred only after 2 hr exposure of the VMN to P, whereas 4 hr were required for a full display of estrous behavior, including solicitation. In Experiment 2, P was lowered into the brain for either 1, 2, or 4 hr, and testing took place 4 hr after the lowering of the implant. It was found that 2 hr of P exposure was sufficient to facilitate full estrous responsiveness at 4 hr. In Experiment 3, it was revealed that the duration of estrous responsiveness was directly related to the time the P implant remained in the brain. In the fourth experiment, the time course of P retention in brain tissue, revealed by determination of 3H-progesterone levels in hypothalamus, agreed with the behavioral findings. Progesterone levels in the region of the VMN remained high while a P implant was in place, but declined rapidly after removal. A dual mechanistic hypothesis for P action in the facilitation of estrous behavior is presented.

Animals↗
PubMed1987

Role of the ultrasonic vocalization of the female rat (Rattus norvegicus) in sexual behavior.

Both male and female rats vocalize ultrasonically during mating. Whereas male calls are known to facilitate female proceptive behavior, the female mating call has not been studied beyond spectrographic analysis. In this article, a series of experiments were done to examine the effects of the female's mating call on rat mating behavior. In the first experiment, females copulated with intact males before and after surgical devocalization. In the second experiment, intact females copulated twice with a male: once when they were able to hear and once when they were temporarily deafened with a medical ear mold. In the third experiment, tape recorded ultrasounds were placed in the presence of devocalized females while they were copulating with intact males. In the control condition, tape hiss was presented. In each experiment, it was observed that the female darted more if communication were disrupted (i.e., female devocalized or male deafened). Playback partially reduced darting to control levels. No other behavior was affected consistently across all experiments. Female calls might facilitate self-regulation of mating behavior, or they might focus the male's attention on her proceptive behaviors. It is also possible that the female calls could alter the stimulus properties of the male's behavior, indirectly affecting her own behavior.

Animals↗
PubMed1986

Antagonism of female sexual behavior with intracerebral implants of antiprogestin RU 38486: correlation with binding to neural progestin receptors.

The steroidal antiprogestin 17 beta-hydroxyl-11 beta-(4-dimethylaminophenyl)-17 alpha-(1-propynl)estra-4,9-dien-3-one (RU 38486) was administered systemically or was implanted into the ventromedial hypothalamus and other brain regions (habenula, preoptic area, interpeduncular region, in order to determine whether the compound could antagonize progesterone (P) activation of estrous responsiveness and whether the compound would exert its behavioral effects at the presumed site of P action and/or at other neural sites implicated in the regulation of female sexual behavior. RU 38486 (5 mg) administered sc 1 h before 200 micrograms P inhibited P facilitation of lordosis behavior in estrogen-primed rats. Intracerebral application of RU 38486 to the ventromedial hypothalamus reduced lordosis responses in 14 of the 25 animals tested. Similar implants in the habenula also inhibited lordosis in 5 of the 14 animals tested. Antiprogestin implants in the interpeduncular region and preoptic area were virtually without effect (1 of 7 inhibited in each group). Interactions of RU 38486 with steroid binding sites in the hypothalamus-preoptic area (HPOA) were also assessed. RU 38486 appeared to be a competitive inhibitor of progestin ([3H] R5020) binding in HPOA cytosols. Scatchard analysis of [3H]RU 38486 binding showed that when unlabeled P was used as the competitor to assess nonspecific binding, the antiprogestin bound with high affinity [dissociation constant Kd = 8.4 nm] to brain cytosols. In addition, the number of [3H]RU 38486 binding sites in HPOA cytosol increased by approximately 50% in estrogen-primed female rats. Competition studies indicated that unlabeled RU 38486 was the most effective competitor for [3H]RU 38486 binding but that P and R5020 were nearly as effective. Corticosterone, hydrocortisone, deoxycorticosterone, and triamcinolone also competed for [3H]RU 38486 binding but were somewhat less effective than the progestins. Testosterone and estradiol did not displace [3H]RU 38486 except at very high molar excesses. Thus RU 38486 appears to bind with highest affinity to HPOA progestin receptors, but it also binds to glucocorticoid receptors. These data are consistent with the interpretation that inhibition of estrous responsiveness by RU 38486 is associated with the antagonist's interference with brain progestin binding.

Animals↗
PubMed1985

Intrahypothalamic effects of progestin agonists on estrous behavior and progestin receptor binding.

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.

20-alpha-Dihydroprogesterone↗
PubMed1985

Effects of prenatal exposure to morphine on the development of sexual behavior in rats.

Females exposed to morphine sulfate in utero (5-10 mg/kg twice a day on days 11-18 of gestation) displayed precocious vaginal opening and had increased body weight from the 8th week after weaning. In addition, there was a substantial inhibition in adult feminine sexual behavior. Male rats that received either morphine or saline prenatally did not show any body weight differences, and most of the measures of masculine sexual behavior did not differ between the two groups. However, the male rats exposed to morphine had a significantly shorter post-ejaculatory intromission latency than the saline controls. Examination of cytosol estrogen receptor levels in the hypothalamus-preoptic area (HPOA) of both saline and morphine sulfate-treated female rats revealed essentially identical patterns of depletion and replenishment. Additionally, estrogen treatment was equally effective at inducing HPOA progestin receptor synthesis in both groups. These results show that prenatal morphine treatment at the times and dose level administered disrupts the development of reproductive function in females but has only minor effects on male reproductive function.

Animals↗
PubMed1984

Progesterone in the ventromedial hypothalamus of ovariectomized, estrogen-primed rats inhibits subsequent facilitation of estrous behavior by systemic progesterone.

The putative neural target sites of progesterone's (P) inhibitory influence on estrous behavior were re-examined utilizing intracranial hormone implants. Subjects were estrogen-primed ovariectomized, Long-Evans rats, and all were outfitted with permanent indwelling guide cannulae aimed for the ventromedial hypothalamus (VMH), preoptic area (POA), or midbrain. In a series of 4 weekly testing paradigms, the ability of blank or P-filled implants to both facilitate estrous responsiveness and to interfere with an animal's ability to exhibit estrous behavior following a systemic injection of P 24 hours later was assessed. P-filled implants placed bilaterally into the VMH inhibited the subsequent facilitation of estrous behavior by systemic P administration. Neither P-filled implants in other brain regions nor blank implants lowered into the VMH had this same effect. Seven of the females that exhibited progesterone-induced behavioral refractoriness 24 h after P stimulation of the VMH exhibited facilitation of estrous responsiveness in behavioral tests given 4.5 h after cannulae placement suggesting that progesterone may exert its facilitative and inhibitory actions on estrous responsiveness at the same neuroanatomical locus.

Animals↗
PubMed1984

Antagonism of central estrogen action by intracerebral implants of tamoxifen.

In order to determine the neural site(s) of estradiol (E2) priming of receptive behavior in female Long-Evans rats, we attempted to inhibit the behavioral effects of peripheral injections of E2 by administering the E2 antagonist tamoxifen (TX) to particular brain regions. Crystalline TX was administered unilaterally or bilaterally via 28-gauge cannulae into the ventromedial hypothalamic nucleus (VMN), the preoptic area (POA), or the interpeduncular region (IP) 1 hr prior to the first of three daily E2 benzoate injections. Subjects were tested for the presence or absence of behavioral estrus 5 hr after a 200-micrograms progesterone injection given 4 days after the initial hormone treatment. Results of this experiment showed that TX inhibits lordosis when directed toward the VMN, but not when directed toward the POA or IP. The quality of the lordosis response and the proportion of subjects showing solicitation behavior were both lower in VMN subjects treated with TX than in POA or IP subjects given the same treatment. Unilateral implants were as effective as bilateral implants in inhibiting the behavior of VMN subjects. A second experiment measured uptake of radiolabeled E2 by nuclei of hypothalamic (HYP) and POA tissue following bilateral TX administration to the VMN or POA. TX was capable of inhibiting uptake of [3H]E2 into nuclei of cells located near the implant site. Most subjects which showed behavioral inhibition also showed a reduction in uptake of [3H]E2 by HYP tissue. These data support the hypothesis that exposure of the VMN to E2 is necessary for the priming of estrous behavior in the female rat.

Animals↗
PubMed1984

Do pup ultrasonic cries provoke prolactin secretion in lactating rats?

Marked prolactin (PRL) secretion in response to the ultrasonic distress vocalizations of rat pups in lactating dams deprived of their pups for 6 hr was reported by others. In two experiments, this phenomenon could not be confirmed under our testing conditions at either 1 or 2 weeks postpartum, although behavioral responses to the ultrasounds were noted. In addition, suckling-induced PRL secretion did not differ consistently as a function of the tape recording (pup ultrasounds, 45 kHz artificially produced ultrasounds, or blank tape) heard prior to the return of pups. The functional significance of rat pup ultrasounds is considered.

Animals↗
PubMed1984

Brain monoaminergic control of male reproductive behavior. I. Serotonin and the post-ejaculatory refractory period.

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.

5,7-Dihydroxytryptamine↗