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R S Bridges

Publications and source records attributed to R S Bridges.

At least 55 records · Page 3Linked to original sources

Long-term effects of parity on opioid and nonopioid behavioral and endocrine responses.

Parity (number of parturitions) affects the endogenous opioid system. Multiparous lactating rats are less sensitive to the effects of morphine (MOR) on maternal behavior (MB) and analgesia than primiparous lactating rats. In order to determine whether these changes in opiate sensitivity persist beyond the lactational state, the present study compared the sensitivity of ovariectomized nulliparous and nonlactating primiparous rats to MOR's effects on MB (Experiment 1), analgesia (Experiment 2) and prolactin release (Experiment 3) in addition to stress-induced analgesia (Experiment 2). In Experiments 1 and 2 primiparous rats were allowed to give birth and remain with their litter (culled to 6 pups) until weaning. At that time the pups were removed and the dams and age-matched nulliparous rats were ovariectomized. Four weeks later animals were exposed to foster pups daily in order to induce MB (Experiment 1). On day 5 or 6 of full MB the primiparous and nulliparous rats received either saline or one of four doses of MOR (0.625, 1.25, 2.5, or 5.0 mg/kg, SC) and 60 min later MB was assessed. MOR, at the 2.5 mg/kg dose, disrupted MB in a significantly greater percentage of nulliparous as compared to primiparous animals (100% vs. 55%, respectively). In Experiment 2, nulliparous and nonlactating primiparous animals received 2.5 mg/kg of MOR four weeks after ovariectomy. Analgesia was assessed on a tail-flick apparatus 30, 60, 90, 120 and 150 min postinjection. One week later the same animals were exposed to cold-water swims (CWS, 2 degrees C, 3.5 min) and tail-flick latencies were again recorded.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗

Alterations in luteinizing hormone-releasing hormone release from the mediobasal hypothalamus of ovariectomized, steroid-primed middle-aged rats as measured by push-pull perfusion.

The spontaneous luteinizing hormone (LH) surge on proestrus as well as the steroid-induced LH surge and hypersecretion of LH following ovariectomy are attenuated in middle-aged female rats when compared to their young counterparts. It is generally assumed that the lower titers of serum LH measured in aging animals result, in part, from age-related alterations in luteinizing hormone-releasing hormone (LHRH) neurosecretion, yet no direct measurements of LHRH release from the hypothalamus of aging females are currently available. The present study utilized the push-pull perfusion technique to characterize and compare in vivo LHRH output from the mediobasal hypothalamus of ovariectomized middle-aged and young females during a steroid-induced LH surge. Twelve-minute perfusates were collected for a period of 6 h from middle-aged and young animals outfitted with push-pull cannulae resting in the mediobasal hypothalamus in close proximity to the median eminence. The overall pattern of LHRH release differed in the two age groups. Mean levels of LHRH measured in brain perfusates from middle-aged females were significantly lower than mean levels measured in young animals. Moreover, mean levels of LHRH detected in perfusates during the 1- and 2-hour intervals prior to and the 1-hour interval after the time of maximal LHRH output were lower in middle-aged animals, and a larger percentage of samples from middle-aged females contained levels of LHRH below the detectability of the assay. The mean amplitude of identified LHRH pulses and maximal LHRH output, however, did not differ in the two age groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

Prolactin modulation of the maternal-like behavior displayed by juvenile rats.

Reports of elevated prolactin (Prl) levels in juvenile rats of the same strain and approximate age, together with the established role of Prl in maternal behavior in adult female rats, prompted us to examine the possible involvement of Prl in the expression of maternal-like behavior in juvenile Sprague-Dawley males and females. Experiment 1 showed that at 25 days of age both sexes exhibited a rapid onset of full maternal behavior (FMB), with males (median = 2.0 days) responding significantly more quickly than females (median = 4.0 days). Moreover, blood sampled for Prl revealed that males had significantly higher levels of circulating Prl than females, (21.0 vs 10.4 ng/ml, respectively). In Experiment 2, CB-154 treatment significantly delayed the onset of FMB in males only, causing latencies to increase to 5.0 days vs 2.0 days for Controls. Female latencies were unaffected by CB-154, 7.0 and 7.5 days for CB-154 and Control groups, respectively. A second set of both male and female juveniles was treated with either CB-154 or vehicle. CB-154 reduced Prl levels in both sexes. In the Controls, the sex difference in Prl levels (males greater than females) was again evident. In Experiment 3 juvenile males were treated with either ovine Prl (0.5 mg) + CB-154, CB-154 + Vehicle, or Vehicle + Vehicle and tested for FMB. Males treated with Prl + CB-154 required 3.0 days to exhibit FMB, significantly faster than CB-154 + Vehicle males which responded in 8.0 days. The response of Vehicle + Vehicle males was intermediate, with a latency of 5.0 days. These results provide support for the idea that Prl is involved in the maternal-like responsiveness shown by 25 day old juvenile males, but that in females a maturational factor may have prevented both heightened responsiveness to pups by 25 days of age and sensitivity to the Prl releasing mechanism(s)/Prl feedback involved in the exhibition of maternal behavior.

Animals↗

Prenatal stress and maternal behavior in intact virgin rats: response latencies are decreased in males and increased in females.

The repeated findings that levels of various male-typical behaviors (e.g., copulatory behavior and intermale aggression) are reduced in prenatally stressed (P-S) males, coupled with reports of effects on female physiology and behavior, prompted us to examine the maternal behaviors of P-S animals toward young. Sprague-Dawley female rats were timed-mated (+ sperm = Day 1). From Gestation Days 15 to 22 experimental females were subjected to heat and restraint stress. Control females remained undisturbed throughout pregnancy. The offspring, as adults, were assessed for maternal behavior. P-S males exhibited a significantly shorter latency (in days) to show full maternal behavior (FMB) than Control males, median = 5.0 vs 8.0, respectively. P-S females, on the other hand, exhibited a significantly longer latency than Control females to show FMB (7.0 vs 3.0, respectively). as well as longer latencies to retrieve one, two, or three pups, to begin to crouch over pups, and to build nests in response to young. Sex differences were apparent between Control males and Control females (females were more responsive to young). In contrast, P-S males and Control females exhibited similar latencies to show components of FMB (3-5 days), as did P-S females and Control males (7-9 days). These data demonstrate, therefore, that prenatal stress eliminates the sex difference normally observed in pup-induced maternal behavior. Moreover, the data suggest that prenatal stress renders the male's responsiveness to young more "female-like," while conversely rendering the response of the female more "male-like."

Animals↗

Growth hormone is secreted by ectopic pituitary grafts and stimulates maternal behavior in rats.

The onset of maternal behavior at parturition in rats is hormonally regulated. Recently, we reported that treatment of behaviorally inexperienced, hypophysectomized (hypox), ovariectomized (ovx) rats with a sequential steroid treatment of progesterone (P) and estradiol (E2), and either ectopic anterior pituitary grafts or prolactin (PRL), stimulated maternal responsiveness toward foster young. That growth hormone (GH) has a number of PRL-like activities led us to ask whether the actions of PRL on maternal behavior were specific to PRL or might be shared by other PRL-like protein hormone, i.e., GH. In Experiment 1 we quantified plasma concentrations of GH and PRL by RIA in groups of hypox female rats that were ovariectomized and treated with a combination of ectopic pituitary grafts (Days 1-23) and Silastic capsules filled with P (Days 1-11) and E2 (Days 11-23). Blood samples were collected from Days 1 to 23 of treatment. Both plasma PRL and GH levels increased after grafting, initially rising 10- to 60-fold by Day 4 and gradually declining throughout the remainder of the 23-day sampling period. Throughout the 3-week period after grafting plasma GH levels were as high or higher than those of PRL. In Experiment 2 the behavioral effects of exogenously administered ovine (o)-GH were measured in groups of hypox, ovx rats that were treated with P and E2 as in Experiment 1. Experimental rats were injected twice daily with 0.25 mg oGH beginning on Day 1. Testing for maternal behavior toward foster young was conducted daily from Day 12 to Day 22. In steroid-treated rats, GH treatment stimulated a more rapid onset of maternal behavior (latencies of 3 vs greater than 10 days for vehicle-injected controls). These data indicate that GH, like PRL, is secreted by ectopic pituitary grafts and is capable of stimulating maternal behavior.

Animals↗

Prenatal stress alters morphine- and stress-induced analgesia in male and female rats.

Prenatal stress affects the expression of many opioid-regulated behaviors in adulthood, e.g., aggressive, maternal, regulatory, and sexual. In the present report we examined two forms of analgesia, morphine-induced (opioid receptor-mediated), and stress-induced [cold-water swim (CWS), nonopioid] analgesia in adult prenatally-stressed (P-S) male and female rats to determine whether and to what extent these analgesic responses might be altered. Timed-mated Sprague-Dawley females were exposed to heat and restraint stress (three daily 1/2 hour sessions, 0830, 1230, and 1630 hr) from days 15-22 of gestation. Control animals remained undisturbed throughout pregnancy. Between 120-150 days of age, baseline pain sensitivities were determined using a tail-flick monitor. P-S and Control animals were then exposed to 3.5 min cold-water swims (2 degrees C) and pain thresholds were again determined at 30 min intervals for 120 min. P-S females exhibited significantly lower pain thresholds than Control females at the 30 and 60 min marks, whereas P-S and Control males did not differ. Six to eight days later, analgesia was measured for 180 min following morphine (5.0 mg/kg) administration. P-S females exhibited significantly greater analgesia at each time-point after morphine treatment than Controls. Conversely, P-S males were significantly less analgesic than Control males from 60 to 180 min. These data suggest that prenatal stress alters the status of endogenous opiate systems. Such prenatal stress-induced alterations in opiate function may help account for some of the behavioral effects reported in P-S animals.

Animals↗

Nipple development and pup-induced prolactin release in male rats treated prenatally with the antiandrogen flutamide.

While maternal female rats display increases in circulating prolactin (PRL) concentrations in response to pup exposure, parental male rats fail to show such an increase. One possible explanation for the lack of an acute PRL response in parental male rats is that males do not have nipples and therefore do not receive stimuli from the pups comparable to those experienced by parental female rats. To examine the contribution of nipple presence and possible stimulation, i.e. suckling, in this sexually differentiated endocrine response, male rats were exposed from days 12-15 of gestation to the antiandrogen flutamide. As adults, flutamide-exposed males had nipples. These males and a group of control males were castrated in adulthood and treated with a 21-day hormone regimen (estradiol and progesterone) that effectively stimulates parental behavior in adult rats. Following hormone treatment, mammary tissue from one set of flutamide-treated males was examined histologically to assess nipple and mammary gland development and responsiveness of these tissues to hormonal stimulation. Additional sets of flutamide-treated and control animals were tested for parental behavior. These latter animals were implanted with indwelling atrial cannulae on day 4 of parental behavior and subsequently bled on day 6 in the absence of young and on day 8 after presentation of young. PRL concentrations did not change in either the flutamide-treated or control parental males bled in the presence or absence of young.(ABSTRACT TRUNCATED AT 250 WORDS)

Anilides↗

Parity-associated reductions in behavioral sensitivity to opiates.

Behavioral and physiological responses differ between primiparous and multiparous female rodents. Specifically, multiparous females respond with the full repertoire of maternal behaviors much more rapidly and with greater intensity than their primiparous counterparts. Since opiates inhibit the expression of maternal behavior in postpartum rats and can be reversed by means of the opiate antagonist naloxone, we investigated whether multiparous females would be resistant to the inhibitory effects of opiates on maternal behavior, relative to primiparous females. In Experiment 1 we evaluated the effects of a range of doses of morphine sulfate (MS; 0.625, 1.25, 2.5, 5.0, and 10.0 mg/kg or saline) on maternal behavior in primiparous females on Days 5-6 of lactation. The 5.0 and 10.0 mg/kg doses effectively disrupted maternal behavior, whereas the lower doses were ineffective or only marginally disruptive. In Experiment 2, age-matched female rats were timed-mated and tested for maternal behavior from Day 5 to 13 of lactation, after daily injections of the 5.0 mg/kg dose of MS. On Day 5 of lactation, this morphine treatment eliminated full maternal behavior in 87% of the primiparous animals, but only 37% of the multiparous animals were affected. By Day 10 of lactation, 100% of the multiparous females displayed full maternal behavior after MS treatment, whereas only 69% of primiparous females were responsive. In Experiment 3, analgesic responses were measured both in rats experiencing their initial or second pregnancy, and in postpartum, lactating rats after MS (5.0 mg/kg) administration. Using a tail-flick apparatus to measure analgesia, we found multigravid females to be significantly less analgesic prepartum than primigravid females, suggesting less sensitivity to endogenous opioids.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗

Preoptic area opioids and opiate receptors increase during pregnancy and decrease during lactation.

Opiate receptor and endogenous opioid content were determined in pregnant, lactating, ovariectomized, and ovariectomized and subsequently estradiol- and progesterone-treated adult female rats. Levels of estradiol and progesterone produced by Silastic capsules implanted in animals of the ovariectomized, hormone-treated group were similar to natural levels of those hormones induced during pregnancy. Quantitative receptor autoradiography and radioimmunoassay were used to determine [3H]naloxone binding density and immunoreactive beta-endorphin content, respectively, in the preoptic area of the hypothalamus. Both opiate receptor binding density and beta-endorphin content in the preoptic area varied in the same direction in all experimental groups. The highest levels of both were observed during pregnancy and the lowest levels during lactation. Ovariectomy without subsequent hormone treatment produced intermediate levels of both opiate receptor and beta-endorphin. Ovariectomy with experimentally-induced estradiol and progesterone levels similar to those of pregnancy produced opiate receptor density and beta-endorphin content similar to those observed in pregnant animals. These data suggest that gonadal steroids are capable of altering function of the endogenous opiate system in the preoptic area. Moreover, preoptic area levels of opioids and opiate receptors are normally elevated during pregnancy and reduced during lactation. Since opiates are known to disrupt ongoing maternal behavior, a reduction of preoptic opiate function during lactation may be required to promote normal maternal behavior. The specific preoptic region involved in opiate regulation of maternal behavior may be illustrated by the zone of opiate receptor alteration observed herein.

Animals↗

Prenatal stress reduces estradiol-induced prolactin release in male and female rats.

Prenatal stress is a potent disruptor of the normal course of sexual differentiation, affecting both males and females. In the present study, we wished to examine a sexually dimorphic endocrine response, estradiol (E2)-induced prolactin (Prl) release, in prenatally-stressed (P-S) males and females. Sprague-Dawley female rats were timed-mated (+ sperm = Day 1). From gestation days 15-22 one group of females was subjected to a thrice-daily regimen of heat and restraint stress (0830, 1230, and 1630 hr) consisting of placing the rats into a Plexiglas restraint tube over which were poised two 100 W floodlights. Control females remained undisturbed throughout pregnancy. At parturition all offspring were cross-fostered to untreated, recently-parturient dams and weaned at 25 days of age. Separate groups of P-S and Control males and females were gonadectomized and, for males, paired testes weights and body weights were recorded. Four days later the animals were implanted with Silastic capsules containing E2, and fitted with intra-atrial cannulae. The following day, blood samples were taken at 0900, 1300, 1500, and 1700 hr for a total of five days. Beginning with the 1700 hr sample on Day 2, and with the exception of the 1500 hr sample on Day 3, P-S males had significantly lower plasma Prl values than Control males through Day 4, and at the 1500 hr sample on Day 5. Moreover, at no point did P-S males exhibit a significant daily afternoon increase in Prl values, whereas Control males did so on Days 2 and 4.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Regulation of prolactin secretion in parental rats: roles of steroid priming and pituitary responsiveness.

Whereas prolactin (PRL) release increases in female rats as a result of stimuli from rat young, parental male rats fail to show a rise in plasma PRL levels in response to pup stimuli. In the present study, we have characterized two aspects of the endocrine control of PRL release in male and female rats in an attempt to account for this sex difference in pup-induced PRL secretion. First, we compared the patterns of PRL secretion throughout a prolonged steroid priming treatment that effectively stimulates the onset of parental responsiveness in both sexes. Second, we measured pituitary responsiveness to a PRL releasing agent (thyrotropin releasing hormone: TRH) in male and female rats that had previously experienced the steroid treatment. We found that in the presence of estradiol alone or soon after the onset of progesterone treatment in the presence of estrogen, female but not male rats displayed afternoon elevations in PRL. We also found that, following steroid treatment, TRH caused significant and comparable elevations in plasma PRL in both sexes. These experiments demonstrate differences in patterns of PRL secretion in male and female rats during the early phase of a steroid priming treatment that induces parental responsiveness, yet comparable pituitary sensitivity to TRH-induced PRL release following this 3 week steroid treatment. These data suggest that sex differences in pup-induced PRL secretion in rats do not result from fundamental differences in endocrine priming or from sex differences in pituitary responsiveness.

Animals↗

Hormonal regulation of maternal behavior in rats: stimulation following treatment with ectopic pituitary grafts plus progesterone.

Changes in hormone secretions during pregnancy help to stimulate the onset of maternal behavior at parturition. To date, studies have demonstrated that estradiol (E2) appears to be a necessary component in the hormonal induction of maternal behavior in rats and other mammals. In the present study, we have reevaluated the contribution of E2, progesterone (P), and hormone-secreting pituitary grafts in the rapid induction of maternal behavior by measuring the behavioral effects of exposure to various combinations of P and prolactin-secreting ectopic pituitary grafts in the absence of estrogen. Adult hypophysectomized and nonhypophysectomized nulliparous rats were ovariectomized 2-3 days (Treatment Day 1) after their arrival in our laboratory. In Experiment #1, experimental, hypophysectomized rats were implanted s.c. with 6 P-filled Silastic capsules and given 2 anterior pituitary (AP) glands that were grafted beneath the kidney capsule on Treatment Day 1. Controls were given blank implants and were sham-grafted. P-filled and blank Silastic capsules were removed on Day 11, and behavioral testing was conducted once-a-day beginning on Day 12 for eleven days. Animals treated with P-plus-pituitary grafts displayed full maternal behavior significantly faster than did controls (median latencies of 3.0 and 7.5 days, respectively). In Experiment #2, nonhypophysectomized rats were assigned to one of three treatments. On Treatment Day 1, one group of rats received 6 P-filled Silastic implants and had 2 AP glands grafted under their renal capsules. A second group of animals received 6 P capsules and was sham-grafted, while controls were given blank implants and were sham-grafted.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Immunoreactive beta-endorphin concentrations in brain and plasma during pregnancy in rats: possible modulation by progesterone and estradiol.

Changes in opioid concentrations in brain and plasma as well as opioid activity have been reported to occur as a function of pregnancy and lactation in rats. The present study examines the status and steroidal regulation of the endogenous opioid, beta-endorphin, in the behaviorally and neuroendocrinologically important preoptic area (POA) and hypothalamus, and in the plasma of pregnant and nonpregnant rats. In the first study, concentrations of beta-endorphin-like immunoreactivity (beta-EP-LI-Ir) in POA and hypothalamic tissues as well as in plasma were measured throughout gestation in rats. beta-EP-LI-Ir concentrations in the POA were significantly higher in rats from day 6 to 18 of gestation than in nonpregnant, diestrous females. beta-EP-LI-Ir concentrations in the POA declined significantly between day 18 and 22 of gestation. Changes in hypothalamic beta-EP-LI-Ir concentrations were not detected either as a function of pregnancy or during pregnancy, while plasma beta-EP-LI-Ir concentrations declined gradually from day 6 to 18 of pregnancy and then increased significantly prepartum (day 22 of gestation). In the second study, the effects of 2 weeks of exposure to pregnancy levels of progesterone and estradiol on brain and plasma beta-EP-LI-Ir were measured. Exposure to the combination of progesterone and estradiol (administered subcutaneously via Silastic capsule implants) resulted in a significant increase in beta-EP-LI-Ir concentrations in the POA, but did not affect beta-EP-LI-Ir concentrations in either the hypothalamus or plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Estrogen binding in nuclear and cytosolic extracts from brain and pituitary of middle-aged female rats.

Estrogen binding was compared in brain and pituitary of long-term ovariectomized young and middle-aged (MA) female rats. Binding was quantified in both cytosolic and nuclear extracts to ascertain whether fractions of estrogen binding are altered in MA females. Estrogen binding detected in nuclear extracts from hypothalamus/preoptic area and anterior pituitary of MA females was significantly lower than levels detected in young females. In each case where an age-related decrease in nuclear estrogen binding was observed, an increased number of putative estrogen receptors was detected in the cytosolic extract. Therefore, the age-related decrease in nuclear estrogen binding did not appear to result from a simple decrease in total available cellular estrogen receptors. Rather these results suggest a decrease in the ability of putative estrogen receptors in aging females to remain tightly bound to nuclei after their isolation. The ability of estrogen receptor complexes from aging animals to bind to DNA was evaluated by DNA-cellulose chromatography in order to examine possible quantitative or qualitative differences in estrogen binding proteins with age. The data did not indicate that the properties of estrogen receptors themselves changed with age. It is possible, therefore, that age-related alterations may interfere with the interaction between the estrogen receptor complex and the nucleus.

Aging↗

Opiate involvement in postpartum aggression in rats.

Opiates and the endogenous opioids mediate maternal behavior and various forms of aggression. The present study sought to investigate the role of opiates in postpartum aggression (PPA), an intense form of agonistic behavior displayed by lactating females. Primiparous rats were screened for their PPA against adult males on day seven postpartum. They were then randomly assigned to one of four treatment groups [morphine, 5.0 mg/kg; naloxone alone, 0.5 mg/kg; morphine (5.0 mg/kg) plus naloxone (0.5 mg/kg); and saline] and tested for PPA on postpartum days eight and nine following the respective treatments. Morphine significantly lowered PPA, and naloxone antagonized the effect. Whereas the morphine plus naloxone, naloxone alone, and saline groups exhibited higher levels of PPA than that shown by the morphine group, there were no differences in PPA found among the morphine plus naloxone, naloxone alone, or saline groups. These results, in conjunction with evidence describing the state of the endogenous opioid system in the postpartum rat, suggest that some aspect of the endogenous opioid system may be involved in another form of maternal behavior, postpartum aggression.

Aggression↗

Length of prolactin priming differentially affects maternal behavior in female rats.

Prolonged exposure to prolactin (Prl) or to ectopic pituitary grafts that secrete Prl has been shown to stimulate maternal behavior in steroid-treated, hypophysectomized female rats. Since Prl levels in the blood of pregnant rats increase beginning 2-3 days prepartum, it was of interest to determine whether acute Prl priming prior to exposure to rat young would also stimulate full maternal behavior. Hypophysectomized, ovariectomized nulliparous rats were assigned to one of three treatments: Group 1, prolonged Prl; Group 2, acute Prl; or Group 3, controls/no Prl. All groups were implanted with 3 X 30 mm progesterone (P)-filled Silastic capsules s.c. at the time of ovariectomy (ovx) on Treatment Day 1. After ovx, Group 1 rats (prolonged Prl) were injected twice daily with 0.5 mg Ovine (o) Prl throughout the course of the study. Group 2 (acute Prl) and 3 (controls/no Prl) females were injected with vehicle alone or noninjected from Day 1-10. On Day 11 of Treatment, P implants were removed from all rats and each female was given a 2 mm estradiol-17 beta (E2)-filled Silastic implant. Starting on Day 11, Group 2 females were injected twice daily with oPrl. Group 3 rats continued to receive vehicle only. Behavioral testing began on Day 12 and was conducted daily through Day 22. Prolonged Prl priming (Group 1) stimulated a rapid onset of all aspects of maternal behavior (latencies less than 1 day, all p less than 0.05-0.001 vs. Group 3 controls). Control latencies ranged from 4-10 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Prolactin stimulation of maternal behavior in female rats.

Inexperienced, hypophysectomized female rats treated with steroids were used in experiments to investigate the roles of the pituitary gland and prolactin in the expression of maternal behavior. Administration of ovine prolactin or treatment with ectopic pituitary grafts, which release prolactin into the circulation, stimulated maternal care in these females toward rat young. Steroid treatment alone, while stimulating maternal behavior in rats with intact pituitary glands, did not facilitate maternal responsiveness in hypophysectomized females. These findings indicate a stimulatory behavioral role for pituitary prolactin in the establishment of maternal care and suggest that exposure to prolactin during pregnancy helps to stimulate the immediate onset of maternal behavior at parturition.

Animals↗

Plasma prolactin levels in parental male rats: effects of increased pup stimuli.

The effects of pup exposure on plasma prolactin (PRL) levels were measured in unrestrained, steriod-primed, orchidectomized parental rats. Castrated adult male rats were treated with estradiol and progesterone for 3 weeks and then exposed to rat young until parental behavior was induced. Blood samples were then collected from parental males in both the presence and the absence of pups. Samples were obtained through the use of indwelling cannulas connected via polyethylene tubing to syringes located outside each subject's cage. Despite the intense pup stimulation provided by exposure to nine rat pups, acute rises in plasma PRL levels were not observed in these unrestrained parental male rats. Parental male rats, therefore, do not appear to have the capacity to secrete prolactin in response to acute exposure to young.

Animals↗