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Biomedical subjects

R S Bridges

Publications and source records attributed to R S Bridges.

At least 73 records · Page 4Linked to original sources
PubMed1985

Hypothalamic LHRH in aging rats: effects of ovariectomy and steroid replacement.

Hypothalamic LHRH was measured by RIA in young and middle-aged (MA) female rats in several endocrine conditions. Temporal alterations in LHRH content associated with the steroid induced gonadotropin surge were compared in medial basal hypothalamic and anterior hypothalamic-preoptic area fragments of ovariectomized young and MA subjects. LHRH content was also compared in ovariectomized, untreated subjects from the two age groups. Finally, LHRH content in MA constant estrous females was compared with content in young females on the morning of proestrus. In all conditions, LHRH levels in both brain regions of MA females were similar to, or significantly elevated above levels measured in young females, yet both the steroid induced surge and the castration induced hypersecretion of gonadotropins were markedly attenuated in aging females. Because studies have verified the responsiveness of the pituitary of MA rats to LHRH, the data suggest that adequate amounts of hypothalamic LHRH do not reach the pituitary. Rather, high levels of hypothalamic LHRH measured in MA subjects may represent accumulation of the peptide in LHRH neurons due to an age-related impairment in release.

Aging↗
PubMed1984

Disruption of ongoing maternal responsiveness in rats by central administration of morphine sulfate.

The ability of central morphine administration to disrupt established maternal responsiveness in rats was examined. Studies focused on the direct administration of morphine sulfate (M) to the preoptic area (POA), a region known to be involved in the expression of maternal behavior in this species. In the first experiment, crystalline M was administered via bilateral 28 g cannulae to the POA or ventromedial hypothalamus (VMH) of 31 ovariectomized, estrogen-primed, nulliparous, pup-induced, maternal females. All subjects were tested twice for maternal responsiveness; once after M-filled cannulae and once after blank inserts were lowered into place. Behavioral tests lasted for 1 h after foster young were introduced into the test cage, and retrieval, grouping and crouching responses were recorded. Thirteen of 14 females with cannulae placements in the POA showed disruption of maternal responsiveness following morphine treatment. In contrast, only 4 of 17 females with VMH implants showed some deficit in maternal behavior following opiate administration. Results of a second experiment established that M-filled implants placed in the POA of lactating females were capable of disrupting the responsiveness of nursing females toward their own young. Finally, the specificity of morphine's central effects were examined in a third experiment in which lactating females received bilateral POA infusions of morphine (0.5 microgram, n = 7), dextrorphan (an inactive stereoisomer of an active opioid compound; 1.0 microgram, n = 7) or saline alone (n = 6). Whereas maternal behavior was disrupted in all morphine-treated subjects, infusions of dextrorphan or saline had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Immunoreactive forms of luteinizing hormone-releasing hormone in the brains of aging rats exhibiting persistent vaginal estrus.

The luteinizing hormone-releasing hormone (LHRH) system in middle-aged female rats exhibiting persistent vaginal estrus (PVE) was examined using immunocytochemical (ICC) techniques. Three LHRH antisera (A-R419, A-R744, A-R422; generously supplied by Dr. A. Arimura) directed toward different portions of the LHRH molecule were utilized to compare the immunoreactive molecular moieties of this hypothalamic peptide present in neurons of aging and young female rats. The immunoreactive forms of the decapeptide detected within neurons of young cycling animals were present within the same regions of the LHRH neurons of PVE females. Immunoreactive LHRH perikarya and fibers in the middle-aged anovulatory females did not differ in their distribution in the basal forebrain from those of young cycling females. Furthermore, no gross morphological differences were apparent at the light microscopic level in LHRH neurons from young and aging females. Of particular importance was the apparent presence of the physiologically active form of the mature decapeptide in terminal regions of the median eminence. These data lead us to propose that failure to release adequate amounts of LHRH from neurovascular terminals and not the lack of availability of this hypothalamic decapeptide contributes to reproductive decline in aging female rats.

Aging↗
PubMed1984

A quantitative analysis of the roles of dosage, sequence, and duration of estradiol and progesterone exposure in the regulation of maternal behavior in the rat.

The regulation of the onset of maternal behavior in the rat is under hormonal control. This study reports a new endocrine model for the study of the hormonal regulation of maternal responsiveness. The model employs the administration of physiological amounts of the steroids estradiol (E2) and progesterone (P) via Silastic implants to inexperienced nulliparous rats and measurement of the effects of these implants on maternal behavior. In the first two experiments, the levels of E2 and P in the sera of pregnant and hormone-treated rats were measured by RIA. Using known physiological treatments of E2 given in combination with P, the effects of E2 and P on maternal behavior were measured. Treatment with a combination of E2 at all dosages plus P for 2 weeks before P removal and behavioral testing stimulated a fast onset of maternal behavior in ovariectomized nulliparous rats. Exposure for 2 weeks to small E2 implants (1 or 2 mm; approximately 20-30 pg/ml serum) did not affect maternal responsiveness, whereas large E2 implants (10 mm; approximately 110 pg/ml serum) stimulated maternal behavior. P treatment alone had no behavioral effect. Simultaneous removal of E2 plus P before exposure to foster young also resulted in a stimulation of behavioral responsiveness, indicating that the presence of elevated titers of circulating E2 is not a requirement for stimulation to occur. In addition to facilitating a rapid onset of behavior, the quality of the response in steroid-primed rats was similar to that measured in lactating rats in a T-maze test. In another experiment, when female rats were treated with P before E2 administration, maternal behavior was rapidly induced. Thus, P itself can sensitize the female to the behavioral effects of E2. Finally, the duration of steroid-exposure before testing was found to influence maternal behavior. Increased durations of E2 plus P exposure before testing were accompanied by decreased latencies to respond maternally to foster young. These data indicate that during pregnancy, E2 and P prime the female to respond to her young at birth. The intensity of the steroidal priming increases as pregnancy progresses, and this primed potential is subsequently unmasked by the decline in P and the maintenance of E2 secretion around parturition. These findings demonstrate that behavioral processes can be modified in the adult animal as a result of long term changes in endocrine state, i.e. pregnancy.

Animals↗
PubMed1983

Intracerebroventricular administration of oxytocin and maternal behavior in rats after prolonged and acute steroid pretreatment.

The role of oxytocin in the initiation of maternal responsiveness in rats was reexamined. Oxytocin (400 ng in 4 microliters saline) or saline alone was infused into the cerebral ventricular system of ovariectomized steroid-primed virgin females. Subjects received 2 weeks of exposure to ovarian steroids via subcutaneously implanted Silastic capsules (Experiment 1) filled with 17 beta-estradiol (1 mm; from Day 1) and progesterone (15 mm; Days 3-13), or they received a single injection of estradiol benzoate (100 micrograms/kg) 48 hr before intracerebral infusion (Experiment 2). Behavioral testing began immediately after oxytocin or saline administration. Latencies to retrieve, group, and crouch over foster young were scored. Contrary to previous reports, oxytocin did not stimulate a rapid onset of maternal responsiveness. The mean latencies to exhibit pup-oriented behaviors ranged from 2.8 to 5.1 days in all groups, regardless of treatment.

Animals↗
PubMed1983

Opiate regulation of maternal behavior in the rat.

The effects of the opiate agonist morphine, the opiate antagonist naloxone and the weak opiate nonanalgesic dextrorphan on the expression of maternal behavior were investigated in a series of three experiments. In the first experiment treatment of rats with morphine (5 mg/kg, subcutaneously) after ovariectomy and hysterectomy on day 17 of gestation resulted in a disruption in the onset and quality of maternal responsiveness in the homecage and in a T-maze test. The duration of morphine's acute disruptive action was 2-4 hours. In the second experiment concurrent treatment of morphine-injected rats with naloxone prevented the disruptive effects of morphine in both the homecage and T-maze tests. The effects of morphine did not appear to result from a severe alteration in activity levels as measured in an open-field test, although morphine did increase activity slightly by the fifth day of treatment. In the third experiment treatment of rats after ovariectomy plus hysterectomy on day 17 of gestation with dextrorphan failed to disrupt maternal behavior. These results indicate that morphine disrupts maternal behavior through an opiate receptor mechanism, and suggests to us that endogenous opiates may mediate the expression of maternal behavior under certain physiological conditions.

Animals↗
PubMed1983

Sex differences in prolactin secretion in parental male and female rats.

The present series of experiments report the behavioral and endocrine responses of male and female rats to rat young. In the first experiment, the behavioral responses of intact male and ovariectomized female rats to foster young were measured. While both of these groups exhibited most components of parental behavior after four to six days of exposure to rat young, males failed to build good nests and to crouch over the young. In addition significantly more males killed young than did ovariectomized females. In the second experiment, treatment of male and virgin female rats with a 21-day hormone regimen of estradiol and progesterone stimulated an equally rapid onset of parental behavior in both sexes. Latencies to exhibit parental responses were approx. two days for both males and females. Pup killing was virtually eliminated in males by hormone treatment. Although the behavioral responses of hormone-primed males and females were similar, their prolactin responses to the presentation of rat young differed. Pup presentation stimulated an increase in plasma prolactin content in hormone-primed parental virgin females similar, but not identical, to that found in lactating control rats, while plasma prolactin levels in hormone-primed parental males did not rise in response to the presentation of young. These data indicate that a sex difference in neuroendocrine, but not behavioral, responsiveness to young exists between parental males and females.

Animals↗
PubMed1983

Plasma prolactin concentrations in parental male and female rats: effects of exposure to rat young.

The effects of pup presentation on the PRL responses in parental male rats were measured and compared with those in parental virgin and lactating female rats. Blood samples were collected from rats through indwelling intraatrial cannulas after a suckling challenge, i.e. presentation of rat young. Lactating rats showed full parental behavior and characteristic large surges in plasma PRL levels within the first 5-10 min on each day that rat young were presented (days 4, 8, and 12 of lactation). When pups were not presented, PRL rises did not occur. In contrast to the pattern of PRL responses shown by lactating mothers, parental ovariectomized nulliparous female and parental intact male rats failed to show specific increases in PRL in response to pup presentation. Plasma PRL levels in these groups, as in nonparental female and male rats, occasionally rose in response to blood collection rather than to pup presentation alone. Treatment of nulliparous female as well as male rats with estradiol and progesterone Silastic implants for 21 days before the initiation of behavioral testing significantly reduced the latencies of both nulliparous females and males to respond to foster young from about 5 to 2 days. The PRL responses of these steroid-primed groups were quite different. The steroid-primed females exhibited a pattern of PRL responses to pups identical to that found in lactating rats. The steroid-primed parental males, in contrast, failed to show specific increases in plasma PRL levels in response to young. These data demonstrate a sex difference in the hormonal, but not behavioral, responses of male and female rats to young and are suggestive of possible sex differences in the hypothalamic and/or peripheral regulation of pup-induced PRL secretion.

Animals↗
PubMed1983

Thyroid stimulating hormone and prolactin secretion: reduced sensitivity to TRH-stimulated prolactin release after midpregnancy in rats.

Prolactin (PRL) and thyroid stimulating hormone (TSH) plasma concentrations were measured during the latter part of the dark period in early and mid-late pregnancy in the rat. On Days 4-5 and 7-8 of pregnancy, plasma PRL concentrations surged between 22:00 and 06:00 hr and TSH values increased between 22:00 and 02:00 hr. While the TSH pattern was maintained during the second-half of pregnancy, surges in PRL release ceased and PRL levels remained at less than 10 ng/ml. The effects of thyrotropin releasing hormone (TRH) administration on PRL and TSH secretion were then measured to determine whether the second-half of pregnancy is associated with a decrease in sensitivity to an agent that can stimulate PRL release. Injection (iv) of cannulated pregnant rats with a low dosage (20 ng) of TRH stimulated a twofold increase in plasma TSH during both early (Days 5-9) and later (Days 14-18) pregnancy but did not change plasma PRL levels. Treatment with a high dosage (2 micrograms) of TRH induced a sixfold rise in plasma TSH during both phases of gestation. The higher dose of TRH also stimulated elevations in plasma PRL during early and mid-late pregnancy; however, both the absolute increase in the amount of PRL in plasma and the percentage increase over baseline levels were greater from Days 5-9 than from Days 14-16 of gestation. These data indicate that the neuroendocrine sensitivity to factors that stimulate PRL secretion changes as pregnancy progresses, and suggest that nocturnal secretion of PRL and TSH during pregnancy may be regulated, in part, by a common trophic factor.

Animals↗
PubMed1982

Reversal of morphine disruption of maternal behavior by concurrent treatment with the opiate antagonist naloxone.

Rats whose pregnancies were surgically terminated on day 17 of gestation were injected with morphine, morphine plus naloxone hydrochloride, or saline, and then tested for maternal responsiveness toward foster young. Morphine treatment alone significantly disrupted the rate of onset and quality of maternal responsiveness. Concurrent administration of naloxone to morphine-injected rats reinstated the rapid onset of behavioral responsiveness toward foster young, such that the responsiveness of the rats treated with both morphine and naloxone was indistinguishable from that shown by saline-injected controls. The disruptive effects of morphine did not appear to result from a general reduction in activity levels as measured in an open-field apparatus. These findings suggest that the normal onset and maintenance of maternal behavior in the rat may be regulated by endogenous opiates.

Animals↗
PubMed1982

Postpartum luteinizing hormone release and maternal behavior in the rat after late-gestational depletion of hypothalamic norepinephrine.

The effects of depletion of hypothalamic norepinephrine (NE) during late pregnancy on the postpartum ovulatory LH surge, the onset and maintenance of maternal behavior and lactation were examined in adult female rats. Bilateral transections of the ascending noradrenergic pathways (ANP) between days 14 and 17 of gestation resulted in a 70% depletion in hypothalamic NE content when assayed on day 6 postpartum. In spite of this depletion in hypothalamic NE content, a postpartum ovulatory surge of LH was observed in transected rats at 18:00 h on either the day of parturition or 1 day later. The magnitude of the LH surge in experimental animals at this time appeared equal to that of controls. A second group of transected and sham-transected rats was tested for maternal responsiveness postpartum and through day 6 postpartum. Primiparous transected females displayed normal maternal behavior during this period with only minor disruptions in nest-building behavior. The lactational performance of transected rats, however, was inferior to that of sham-transected animals. The hypothalamic content of NE in females that showed impairment of lactation was consistently below the NE content found in the controls. The importance of the noradrenergic system in the control of maternal behavior is discussed, and it is proposed that noradrenergic involvement in maternal behavior is modulatory rather than directly regulatory.

Animals↗
PubMed1981

Steroidal interactions in the regulation of maternal behaviour in virgin female rats: effects of testosterone, dihydrotestosterone, oestradiol, progesterone and the aromatase inhibitor, 1,4,6-androstatriene-3,17-dione.

The effects of exposure to concentrations of androgens, oestradiol (OE2) and progesterone similar to those found during pregnancy on the induction of maternal behaviour were investigated in female rats. In the first experiment the effects of testosterone and dihydrotestosterone (DHT) administered in combination with progesterone (using silicone elastomer capsules) on the induction of behavioural responsiveness towards young (crouching, retrieval and grouping of pups) were measured in ovariectomized virgin rats. Hormonally treated animals were exposed to testosterone or DHT from day 1 of treatment to the end of behavioural testing, while progesterone was administered for 10 days (days 3-13). Testing for maternal responsiveness began on day 14 and lasted until day 23. Significant reductions in latencies to show individual aspects of and complete maternal behaviour were found only in animals treated with a combination of testosterone and progesterone (range of mean latencies for showing one aspect of, to complete, maternal behaviour = 1.0-1.4 days). The mean latencies of the other hormonally treated animals ranged from 5 to 6 days and were similar to those of non-hormonally treated control rats. The second experiment examined the possibility that stimulation of maternal behaviour in animals given testosterone and progesterone resulted from the aromatization of testosterone to OE2. Ovariectomized virgin rats were implanted with capsules containing testosterone and other with the aromatase inhibitor, 1,4,6-androstatriene-3,17-dione (ATD) on day 1, and with progesterone capsules on day 3. Progesterone capsules were removed on day 13 and behavioural testing commenced on day 14. Treatment with testosterone and progesterone failed to stimulate maternal behaviour in rats treated with ATD. In a third study ovariectomized virgin rats were implanted with OE2 on day 1 and progesterone on day 3. The progesterone implants were removed on day 13 and testing began on day 14. Significant reductions in latencies to show all aspects of maternal behaviour were found in these rats. In a final study progesterone capsules remained in OE2- and progesterone-treated rats from day 3 until the completion of behavioural testing. The presence of progesterone implants throughout the test period (days 14-23) blocked the rapid onset of maternal responsiveness induced by removal of progesterone on day 13 shown in rats treated with OE2 plus progesterone in experiment 3. These data suggest that during gestation testosterone, through its conversion to OE2, synergizes with progesterone to help stimulate the development of the capacity of the female animal to respond maternally to young, a capacity unmasked by withdrawal of progesterone before parturition.

Androstatrienes↗
PubMed1979

Effects of transecting lateral neural connections of the medial preoptic area on maternal behavior in the rat: nest building, pup retrieval and prolactin secretion.

In lactating female rats bilateral parasagittal cuts transecting the dorsolateral neural connections of the medial preoptic area (MPOA) abolished nest building and retrieving components of maternal behavior, while crouching and nursing were unaffected. While few animals with these cuts were suckled when presented with pups the prolactin secretion response was undiminished when suckling did occur. Whereas previous studies have demonstrated that extensive surgical separation of the medial preoptic area-anterior hypothalamic continuum from the lateral preoptic area-lateral hypothalamus disrupts all aspects of maternal behavior, the present study has determined more specifically the zone of fibers essential for the active components of maternal behavior, i.e., nest building and retrieving. These fibers appear to enter/leave MPO dorsolaterally beneath the crossing of the anterior commissure in the region of the bed nucleus of the stria terminalis. These neural connections are not the same as those that regulate prolactin secretion in the lactating rat.

Animals↗
PubMed1978

Inhibitory effects of various progestins and deoxycorticosterone on the rapid onset of maternal behavior induced by ovariectomy-hysterectomy during late pregnancy in rats.

The inhibitory effects of progesterone (P), 5 alpha-dihydroprogesterone (5 alpha-DHP), 17 alpha-hydroxyprogesterone (17-HP), and deoxycorticosterone (DOC) upon the rapid onset of maternal behavior induced during late pregnancy in primigravid rats by ovariectomy-hysterectomy (OH) were examined. Progesterone administration at a dosage of 5.0 mg oil vehicle daily (beginning on Day 17 and ending when the subject responded maternally to foster pups) significantly delayed by about 1.5 to 2.0 days the onset of maternal behavior. In contrast, P at dosages of either 1.0 or 2.5 mg daily, 5 alpha-DHP at 5.0 mg administered daily in either an oil or Tween-80 vehicle, 17-HP at 5.0 mg in oil daily, and DOC at dosages of either 5.0 or 10.0 mg in oil daily failed to effect the rapid onset of maternal behavior induced by ovariectomy-hysterectomy on Day 17 of pregnancy. These data suggest that during pregnancy the onset of maternal behavior is inhibited in a rather specific manner by progesterone.

Algestone↗