Biomedical subjects

R S Bridges

Publications and source records attributed to R S Bridges.

At least 19 recordsLinked to original sources

PubMed1992

Neural and endocrine sensitivities to opioids decline as a function of multiparity in the rat.

Hormonal changes during pregnancy regulate the onset of maternal behavior at parturition. In addition, the concentrations of beta-endorphin and mu opioid receptors are higher during pregnancy and lower during lactation. Previous studies have shown that sensitivity of female rats to the disruptive behavioral effects of morphine changes as a function of the number of pregnancies and/or lactations the females undergo. The objectives of the present study were to determine whether central infusions of the endogenous opioid, beta-endorphin, would disrupt maternal behavior. Next, we investigated the possibility that the neural sensitivity to beta-endorphin changes with repeated pregnancies. And finally, we examined whether opioid-mediated endocrine responses also change as a function of multiparity. In the first study, bilateral infusions of low doses (0.06-0.72 nmol) of beta-endorphin into the medial preoptic area (MPOA) of lactating, primiparous rats disrupted maternal behavior. When comparable doses of beta-endorphin were infused into the MPOA of age-matched, multiparous rats, the behavioral effects of beta-endorphin were significantly attenuated. In response to suckling stimulation, an opioid-mediated endocrine response, primiparous mothers secreted more prolactin than did multiparous rats. Moreover, multiparous, but not primiparous, mothers were insensitive to the ability of naloxone, an opiate antagonist, to block suckling-induced increases in prolactin. These findings indicate that reductions in neural sensitivity to opioids develop as females undergo repeated pregnancies and lactations, changes which affect both behavioral and endocrine functions.

Animals↗

PubMed1992

Parity-associated alterations of medial preoptic opiate receptors in female rats.

Preoptic area opiate receptor density was measured by quantitative autoradiography using [3H]naloxone in female rats during their first and second pregnancies and lactations and in a separate group of ovariectomized, nulliparous animals. Opiate receptor density in the medial preoptic area (MPOA) was elevated on day 12 of gestation in both primigravid and multigravid rats when compared with ovariectomized subjects. MPOA receptor density was reduced in primiparous mothers on day 5 of lactation relative to pregnancy. In contrast, receptor density in the MPOA did not decline in multiparous (second lactation) rats relative to pregnancy levels. Opiate receptor density was significantly higher on day 5 of lactation in multiparous than in primiparous mothers. No difference in receptor density was detected in the adjacent lateral preoptic area among the treatment groups. An examination of hormone titers revealed that basal prolactin levels were significantly higher in primigravid than multigravid rats, and that during lactation prolactin titers were negatively correlated with MPOA opiate receptor density in the primiparous mothers. The data demonstrate that multiple pregnancies and lactations result in changes of MPOA opiate receptor density and of circulating hormone levels. The findings are discussed in terms of the concurrent changes in neural opiate sensitivity associated with multiparity.

Analysis of Variance↗

PubMed1992

Domperidone induces a probenecid-sensitive rise in immunoreactive prolactin in cerebroventricular perfusates in female rats.

The present study examined immunoreactive prolactin (ir-PRL) access into the cerebrospinal fluid (CSF) by monitoring ir-PRL levels in the blood and cerebroventricular perfusates of ovariectomized (ovx) rats treated with the dopamine antagonist, domperidone (DOMP). In Expt. 1 PRL plasma levels were measured in rats treated with DOMP i.p. (2.5, 5.0 and 10.0 mg/kg). All doses of DOMP significantly increased PRL plasma levels. In Expt. 2 animals were treated i.p. with DOMP (10 mg/kg) or DOMP plus the active transport blocking agent, probenecid (PROB; 250 mg/kg). Plasma PRL and ir-PRL in cerebroventricular perfusates were measured in separate sets of animals using catheters and a push-pull perfusion system, respectively. DOMP induced an increase in plasma PRL that was followed 30-40 min later by a rise in ventricular perfusates ir-PRL levels. PROB treatment induced a greater increase in plasma PRL levels in DOMP-treated animals, but delayed the DOMP-induced increase in ir-PRL ventricular perfusate ir-PRL levels. The delay in the rise of ir-PRL in ventricular perfusates observed in rats treated with DOMP plus PROB may be due to a PROB's interference with the transport of PRL from the blood into CSF. These results suggest that under some conditions ir-PRL in CSF originates from the pituitary.

Animals↗

PubMed1992

Diminished luteinizing hormone release in prenatally stressed male rats after exposure to sexually receptive females.

Prenatally stressed (P-S) males show reductions in male sexual behavior, medial preoptic area volume, and levels of circulating testosterone. We examined the luteinizing hormone (LH) response to the presence of a sexually receptive female, a known index of sexual arousal. Adult male offspring from mothers stressed on days 15-22 of pregnancy (thrice-daily exposures to heat, light, and restraint) were implanted with an intraatrial catheter. Forty-eight h later they were placed into test chambers divided by a wire mesh partition; the catheter was extended outside the chamber. Thirty min later a baseline blood sample (time 0 min) was taken and a sexually receptive female was then placed on the side of the partition opposite the male for 60 min. Blood samples were collected 5, 10, 15, 30, 60 min, and 24 h after introduction of the female. Prenatally stressed males exhibited significantly lower LH levels following exposure to the female at each time point, 5 min to 24 h. Furthermore, at no point were P-S males' LH levels significantly increased above baseline levels. These data suggest that attenuations in female-induced LH release are associated with the marked reductions in male sexual behavior characteristic of the P-S male.

Animals↗

PubMed1992

Hormonal regulation of medial preoptic mu-opiate receptor density before and after parturition.

Endogenous opioid peptides acting in the medial preoptic area (MPOA) appear to be involved in the regulation of maternal behavior in lactating rats. Moreover, it is known that the density of mu-opiate receptors in the MPOA is elevated during pregnancy, but decreases during lactation. In the first experiment of this study, mu-receptor density in the preoptic area was examined across the periparturitional period on gestation days 18, 20 and 22, at 1 h postpartum and on postpartum days 1 and 12. The effect of pregnancy during lactation on mu-receptor density was also assessed. In addition, plasma hormone concentration of estradiol (E2), progesterone (P), and prolactin (PRL) were determined. While plasma P levels decreased and PRL levels increased prior to parturition, MPOA mu-receptor density remained elevated until 24 h after parturition before declining to reach a level similar to that of ovariectomized control animals. Receptor density was significantly correlated with PRL levels only in gestation day 22 animals, when PRL levels were highest. MPOA mu-receptor density was low at postpartum day 12 whether or not the animal was pregnant. No effects were observed in the adjacent lateral preoptic area in any group. In the second experiment, the effect of hormonal manipulation on preoptic opiate receptor density was examined at various times after removal of Silastic capsules containing P following sustained E2/P exposure. While P levels decreased abruptly following capsule removal, MPOA receptor density declined more gradually. The results are consistent with the hypothesis that a reduction of mu-receptor density occurs in the MPOA following parturition by receptor turnover in the absence of sufficient hormonal stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Intracerebroventricular cholecystokinin infusions block beta-endorphin-induced disruption of maternal behavior.

Recent work has shown that infusions of beta-endorphin, an endogenous opioid, into the ventricular system of lactating rats blocks normal maternal behavior. Other behavioral and biochemical studies have demonstrated that sulfated cholecystokinin-octapeptide (CCK-8) can have effects opposite those of opioids. The present study evaluated whether intracerebroventricular (ICV) administration of CCK-8 is able to antagonize the inhibitory effect of beta-endorphin on maternal behavior. The results of this study demonstrated that CCK-8 (14.5 nmol) prevented the beta-endorphin (1.45 nmol)-induced increase in latencies to retrieve the first pup, retrieve all pups, and to group and crouch over rat pups. In addition, reductions in the percentage of rats retrieving all pups and displaying full maternal behavior were prevented by CCK-8. These data suggest that CCK-8 can act as an opioid antagonist in neural systems that control maternal behavior.

Animals↗

PubMed1991

Opioid receptor subtype involvement in maternal behavior in lactating rats.

Central or systemic administration of morphine disrupts maternal behavior in steroid-primed, pup-induced virgin and lactating rats. Morphine, the prototypical mu agonist, also interacts with different opioid receptor subtypes. The present study examined the effectiveness of five receptor-selective agonists, in addition to morphine, to disrupt maternal behavior in primiparous lactating rats following intracerebroventricular (i.c.v.) infusions in order to characterize opioid receptor subtype involvement in maternal behavior in the female rat. Virgin, Sprague-Dawley rats were mated and implanted with lateral ventricle cannulae on days 13-15 of gestation. On postpartum day 5, mothers were tested for maternal behavior 30 min after i.c.v. vehicle infusion (5 microliters). On day 6, rats received one of the following opioid receptor agonists 30 min before testing: beta-endorphin (mu/epsilon receptor subtype; 0.29, 0.72, 1.45, 2.9 nmol), DAGO (mu; 0.29, 0.72, 1.45, 2.9 nmol), morphine (mu; 0.29, 0.72, 1.45, 2.9, 14.5 nmol), DPDPE (delta; 2.9, 29 nmol), U50488H (kappa l; 2.9, 29, 145 nmol) and SKF10047 (sigma; 2.9, 29, 145 nmol). Only activation of mu opioid receptors dose-dependently disrupted maternal behavior in primiparous lactating rats. DPDPE, U50488 and SKF10047 had no discernible effect on maternal behavior. DAGO, a highly selective mu agonist, was even more potent than beta-endorphin and morphine in disrupting maternal behavior suggesting that maternal behavior is regulated by opioids interacting with the mu opioid receptor.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1990

Prenatal stress has long-term effects on brain opiate receptors.

Prenatal stress has been associated with a number of behavioral consequences including altered sensitivity to exogenous opiates. In the present study, mu opiate receptors were compared in the 42-day-old offspring from females stressed on days 15-22 of gestation and from females who were unstressed controls. Membrane homogenates from the prenatal stress group showed less binding of the mu opiate receptor ligand, [3H]DAGO in striatum but not in several other brain regions. Saturation studies suggest this difference is due to fewer striatal mu opiate receptors in offspring of prenatally stressed females. Using in vitro receptor autoradiography, the decreased binding in striatum was found mostly in the rostral striatum, extending into the nucleus accumbens with conservation of the normal anatomic distribution of receptor rich patches.

Animals↗

PubMed1990

Morphine treatment and reproductive condition alter olfactory preferences for pup and adult male odors in female rats.

Administration of morphine sulfate (MS) to pregnancy-terminated and postpartum lactating female rats disrupts both maternal behavior and postpartum aggression. Since the display of these behaviors may be heavily dependent on olfactory cues provided by the stimulus animals (rat pups and adult male rats, respectively), we examined whether MS was affecting the perception of the olfactory stimuli, and whether olfactory perception was modified by reproductive condition. In Experiment 1, lactating rats had their pups removed and were injected with MS (5.0 mg/kg, sc.) or saline. 60 min later they were placed into a two-choice apparatus, one side of which contained bedding soiled by neonates and the other clean bedding. Time spent on each side was recorded for a total of 5 min (300 s; chance = 150 s). Saline-treated mothers spent significantly more time on the pup-odor side, whereas MS-treated females spent significantly less. In Experiment 2, lactating females were treated with MS or saline and exposed to male odors (soiled bedding). MS significantly increased time spent on the side with male odors; when treated with saline, time spent was significantly reduced. Thus, in lactating rats. MS creates an aversion for pup odors while reducing the female's normal aversion toward male odors. In Experiment 3, ovariectomized (ovx) virgin females expressed neither an aversion nor a preference for the odor of pups following saline administration. After MS treatment, however, the virgins showed a distinct preference for pup odors. When exposed to male odors in Experiment 4 ovx virgins showed a marked preference for male odors after MS treatment, and neither a preference nor an aversion after saline. Experiment 5 examined pup odor preferences in intact virgins, early (Day 7), middle (Day 14), late-pregnant (Day 21), and prepartum (Day 22) rats. The pup odor preferences of virgin, Day 7, Day 14, and Day 21 pregnant rats were not different and generally were at chance levels. Day 22 pregnant females exhibited a marked preference for pup odors compared to chance levels, as well as compared to the other four groups. These findings suggest that opiates and endogenous opioids may regulate olfactory preferences and that alterations in this system may underlie normal behavioral changes toward conspecifics prepartum as well as during lactation.

Animals↗

PubMed1990

Mu 1 opioid receptor involvement in maternal behavior.

Previous studies have demonstrated that morphine inhibits the display of maternal behavior in lactating rats. Whether morphine exerts its actions specifically at the mu receptor has not yet been determined. The present study examined this possibility by evaluating whether naloxonazine, an irreversible and selective antagonist of the mu 1 opioid receptor subtype, is able to attenuate morphine's disruptive effect on maternal behavior in primiparous lactating rats. Experiment 1 compared the ability of naloxonazine (AZINE) and naloxone (NAL) to block the action of morphine (MOR) on maternal care. Virgin, Sprague-Dawley rats were mated in our colony and on day 3 postpartum (parturition, day 0) all rats received jugular catheters. On day 6 the mothers received one of the following treatments: MOR alone (10 mg/kg, SC, N = 10); MOR (10 mg/kg, SC) 24 hr after AZINE pretreatment (10 mg/kg, IV, N = 10); MOR (10 mg/kg, SC) 24 hr after NAL pretreatment (10 mg/kg, IV, N = 8); or MOR (10 mg/kg, SC) immediately after NAL (0.5 mg/kg, SC, N = 10). MOR alone completely disrupted maternal behavior (0% responded) which was blocked by prior NAL administration (100%). AZINE pretreatment 24 hr earlier partially blocked MOR disruption of MB (40% responded; significantly different from MOR alone). The response of rats pretreated 24 hr earlier with NAL did not differ from MOR alone. AZINE blocked MOR's effect on pup retrieval to an even greater degree (70% responded vs. 10% in MOR alone). Experiment 2 determined the ability of AZINE to interfere with varying doses of MOR on maternal behavior.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Central prolactin infusions stimulate maternal behavior in steroid-treated, nulliparous female rats.

A series of experiments were conducted to determine whether and under what conditions central prolactin (PRL) administration would stimulate the onset of maternal behavior in female rats and to identify possible neural sites of PRL action. In each experiment ovariectomized, nulliparous rats whose endogenous PRL levels were suppressed with bromocriptine were tested for maternal behavior toward foster young. In experiments 1, 2, and 4, females were also exposed to pregnancy-like levels of progesterone (days 1-11) followed by estradiol (days 11-17). In experiment 1 infusions (days 11-13) of four doses of ovine PRL (400 ng, 2 micrograms, 10 micrograms, or 50 micrograms, but not 80 ng) into the lateral ventricle resulted in a rapid onset of maternal behavior (behavioral testing, days 12-17). The stimulatory action of these doses of PRL appears to be central, since subcutaneous injections of 50 micrograms of ovine PRL failed to affect maternal responsiveness (experiment 2). Experiment 3 indicated that the stimulatory effect of intracerebroventricularly administered PRL is steroid dependent. Infusions of either 10 micrograms of ovine PRL or 10 micrograms of rat PRL failed to induce maternal behavior in nonsteroid-treated animals. In the final experiment (no. 4) bilateral infusions of 40 ng of ovine PRL into the medial preoptic area of steroid-treated rats resulted in a pronounced stimulation of maternal behavior. These findings demonstrate a central site of PRL action in the stimulation of maternal responsiveness and point to the medial preoptic area as a key neural site for PRL regulation of maternal behavior.

Animals↗

PubMed1990

Prolactin (PRL) regulation of maternal behavior in rats: bromocriptine treatment delays and PRL promotes the rapid onset of behavior.

Recent findings indicate that PRL helps stimulate the onset of maternal behavior in inexperienced hypophysectomized steroid-treated female rats. In a series of five experiments we have further examined the involvement of PRL in maternal behavior using nonhypophysectomized ovariectomized rats treated concurrently (type I) or sequentially (type II) with progesterone (P) and estradiol (E2) and administered either bromocriptine (to suppress endogenous PRL secretion) or bromocriptine plus ovine PRL. In Exp 1 plasma PRL concentrations were measured in ovariectomized rats treated for 2 weeks with a combination of E2 and P Silastic implants. Type I steroid-treated (2mm E2, days 1-24; three 30 mm P, days 3-13) rats exhibited elevated plasma PRL levels throughout the sampling period compared with nonsteroid-treated controls. In contrast, PRL concentrations in type II steroid-treated (P, days 3-13; E2, days 13-24) females were low (similar to controls) from days 3-13 when the type II steroid-treated females were exposed to P only. Like type I treated rats, PRL levels in type II steroid-treated rats were elevated from day 13 onward after E2 capsule insertion. In Exp 2, treatment of both type I and type II steroid-treated rats with bromocriptine (2 mg/kg, sc) twice daily beginning on treatment day 13 suppressed basal PRL concentrations and prevented the estrogen-induced diurnal PRL surge. Whereas PRL was effectively suppressed by bromocriptine in both steroid-treated groups, the absolute levels of PRL were lower in rats treated with the type II steroid regimen. Behavioral analyses in Exp 3, 4, and 5 revealed that bromocriptine administration, while failing to interfere with the onset of maternal behavior in rats treated with the type I concurrent steroid regimen, disrupted the onset of maternal care in rats treated with the type II sequential steroid regimen. When a separate set of type II steroid-treated rats was given both bromocriptine (2 mg/kg) plus ovine PRL (0.5 mg, sc) twice daily, maternal behavior rapidly appeared. Thus, suppression of endogenous PRL secretion delays the onset of maternal behavior in nonhypophysectomized steroid-primed rats, an effect prevented by concurrent administration of ovine PRL. In addition to providing further experimental support for PRL's role in maternal behavior, the development of this endocrine regimen provides researchers with a potentially fruitful model to examine neural sites and mechanisms of PRL regulation of maternal behavior in mammals.

Animals↗

PubMed1989

Alterations in stress-induced prolactin release in adult female and male rats exposed to stress, in utero.

Prenatal stress alters the endocrine as well as the behavioral responses of rodents. Because of the reductions in both estradiol-induced and ether-induced prolactin (Prl) release reported in prenatally-stressed (P-S) rats, we were interested in whether prenatal stress might also modify the prolactin response of male and female rats to a moderate stressor in adulthood, viz., restraint stress. Timed-mated Sprague-Dawley females were exposed to a daily regimen of heat and restraint stress from days 15-22 of gestation. Control animals remained undisturbed throughout pregnancy. In adulthood, half of the male and female P-S and Control offspring were stressed by placing them in a Plexiglas restraint tube for 60 min (restraint stressed; S; referred to as P-SS and CS, respectively). The remaining half of the P-S and Control animals were left undisturbed (these were nonrestrained; NR; referred to as P-SNR and CNR, respectively). Blood samples (decapitation) were then collected from all animals and plasma was assayed for Prl content. P-SNR and CNR males did not differ in baseline Prl levels, nor did P-SNR and CNR females. Following the restraint stress in adulthood, P-SS males as well as PSS females exhibited significantly less of an increase in Prl relative to CS males and CS females, respectively. In addition, baseline Prl levels differed between the sexes, with females--regardless of prenatal condition--having higher plasma Prl levels than males. These sex differences were no longer evident following restraint stress. These data, in combination with other work in P-S animals in the areas of Prl release and stress responses, demonstrate that prenatal stress renders the rat less hormonally (Prl) responsive to stress, with the effect being more pronounced in the female.

Animals↗

PubMed1989

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↗

PubMed1989

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↗

PubMed1988

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↗

PubMed1988

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↗

PubMed1988

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↗