Biomedical subjects

M J Woller

Publications and source records attributed to M J Woller.

14 recordsLinked to original sources

PubMed1996

Changes in percentages of adenohypophysial gonadotrophs associated with the sex-specific, selective increase in serum follicle-stimulating hormone concentration in the juvenile female hamster.

In normal hamsters, we investigated whether the sex-specific, selective increase in serum FSH concentration in the juvenile female was associated with sex-specific changes in the percentages of adenohypophysial gonadotrophs. Serum LH concentrations did not rise between Day 4 and Day 19 in either sex and did not differ significantly between the sexes on Days 4, 7, 12, 14, and 19 after birth. Serum FSH concentrations were about 2-fold higher on Days 7, 12, and 14 than on Days 4 or 19 in males. In females, serum FSH rose markedly between Days 4 and 7, declined slightly by Day 12, rose to peak levels by Day 14, and declined slightly by Day 19 to levels not different from those seen on Day 7. Body weights rose between Days 4 and 19 and were similar in both sexes. There were no sex differences in pituitary gland weights, which rose between Days 4 and 12 and did not increase significantly further by Day 19. On Day 0, the percentages of immunoreactive LH and FSH cells were about 6 and 1%, respectively, in both sexes. These percentages increased progressively between Days 0 and 7 and between Days 7 and 14. On Day 7, but not on Day 14, the percentages of LH and FSH cells were greater in females than in males. There were more LH than FSH cells in males on Days 0, 7 and 14, and in females on Day 0 but not on Day 7 or 14. Matching of 10 FSH cells per gland with LH cells in serial sections of each of 30 glands showed FSH immunoreactivity to occur only in cells staining for LH. In hypophysectomized-gonadectomized adult hamster hosts with allografts of neonatal pituitary glands beneath the renal capsule, we investigated whether these sex-specific changes in the percentage of cells might be predetermined by the time of birth or dependent on sex differences in the internal environment existing in the postnatal hamster. Groups consisted of male donors-male hosts, male donors-female hosts, female donors-female hosts, and female donors-male hosts. The percentages of LH cells in allografts in all four groups increased from Days 0 to 7 and from Days 7 to 14. Percentages of LH cells on Day 14 in all four groups were not different from those in age-matched male or female adenohypophyses in situ. In contrast, the mean percentages of FSH cells were low (about 1-3%) on Days 0, 7, and 14 in all four groups. In other males hosts, administration of a low dose of LHRH for 7 days did not alter the percentage of LH cells in male allografts but increased the percentage of FSH cells to approach that observed in age-matched male adenohypophyses in situ. Administration of a larger dose of LHRH for 7 days to other male hosts with male allografts increased the percentages of LH and FSH cells to percentages not different from those in age-matched female adenohypophyses in situ. Matching of 10 FSH cells/allograft with LH cells in serial sections of each of 58 allografts showed FSH immunoreactivity to occur only in cells staining for LH. The results of experiments conducted on normal hamsters demonstrate that more marked increases in the percentages of adenohypophysial LH cells and FSH cells occur in females than in males in association with the onset of the selective increase in serum FSH levels in females. The results of experiments employing allografts suggest that the greater increase in LH and FSH cells in females is due to sex differences in the internal environment existing in the postnatal hamster, which can be accounted for by differences in LHRH secretion, rather than to inherent differences between female and male adenohypophyses at the time of birth. We conclude that the greater increases in gonadotrophs observed in female hamster pups on Day 7 after birth and the accompanying sex-specific, selective elevation in serum FSH concentration are probably due to sex differences in LHRH secretion during the juvenile period.

Animals↗

PubMed1996

Adenohypophysial allografts releasing prolactin decrease prolactin mRNA concentration in the host hamster's adenohypophysis in situ.

The inhibitory effects of pituitary allografts on the prolactin (PRL)-secretory system are presumed to be consequences of the unabated release of PRL by the allografts. In the present studies we used pituitary allografts in the Golden Syrian hamster to address the following questions: (a) Do allografts of adult adenohypophysial tissue which elevate serum PRL levels decrease the concentration of PRL mRNA in the host's adenohypophysis? (b) Is this effect shared by allografts of neonatal hypophysial tissue or neonatal muscle tissue which do not elevate serum PRL levels? (c) Do any of these types of allograft alter growth hormone mRNA in the host's adenohypophysis? Prolactin mRNA concentration, but not growth hormone mRNA concentration, was decreased in the adenohypophyses in situ in the hosts bearing adult adenohypophysial allografts in which serum PRL levels were elevated. In contrast, serum PRL in hosts with neonatal hypophysial or muscle allografts were not elevated and PRL mRNA levels in the adenohypophysis in situ were not decreased when compared to the levels measured in hamsters with sham transplants. Prolactin mRNA levels in hosts with neonatal muscle allografts were not different from levels in hosts with neonatal hypophysial allografts but were increased when compared to the levels measured in hamsters with sham transplants. There were no differences in PRL concentration in the adenohypophyses in situ between any of the groups. Also, PRL concentrations in neonatal hypophysial allografts were similar to those in adult adenohypophysial allografts. To our knowledge these observations are the first demonstrating that short-loop feed-back of PRL includes a decrease in PRL mRNA concentration. The observations also support the working hypothesis that PRL and not another pituitary factor exerts the negative feedback.

Animals↗

PubMed1995

Induction of cellular follicle-stimulating hormone in the hamster adenohypophysis requires intermittent stimulation by luteinizing hormone releasing hormone.

We investigated the effectiveness of continuous vs intermittent LHRH stimulation of the neonatal female anterior pituitary gland on inducing cellular FSH immunoreactivity in the Golden Syrian hamster. Neonatal female pituitary glands were grafted beneath the right renal capsules of hypophysectomized-ovariectomized adult hosts with a catheter implanted in the external jugular vein. In experiment 1, vehicle or LHRH (6 ng/h) was infused continuously or LHRH was pulsed at 1 h (6 ng) or 12 h (72 ng) intervals through the catheters for 8 days. Hamsters were decapitated for collection of trunk blood shortly after the end of treatment, and grafts were prepared for immunocytochemical staining for LH and FSH. Anterior pituitary glands removed from neonatal (day 1) and day 9 female pups also were stained for LH and FSH. The mean percentage of adenohypophysial cells staining for LH increased from 11% in neonatal pups to mean percentages (24-28%) that were similar in day 9 pups and in all groups with grafts. The mean percentage of adenohypophysial cells staining for FSH increased from 1% in neonatal pups to percentages (16-21%) that were similar in day 9 pups and in grafts in hosts administered 6 or 72 ng LHRH pulses. By contrast, the mean percentage of FSH cells did not increase in grafts in hosts administered vehicle or LHRH by continuous infusion. Serum LH concentration was low in hosts given vehicle or LHRH by continuous infusion but elevated in hosts given 72 ng LHRH pulses and in all but one host given 6 ng LHRH pulses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Neuropeptide Y and luteinizing hormone releasing hormone synergize to stimulate the development of cellular follicle-stimulating hormone in the hamster adenohypophysis.

Luteinizing hormone releasing hormone (LHRH) stimulates the development of cellular FSH immunoreactivity in the perinatal hamster adenohypophysis. Because neuropeptide Y (NPY) can act directly on rat adenohypophysial cells to stimulate FSH and LH release and potentiate the stimulatory effect of LHRH on FSH and LH release, we investigated the effects of NPY alone and in combination with a low, ineffective dose of LHRH on inducing cellular FSH immunoreactivity in the neonatal hamster adenohypophysis. Neonatal female pituitary glands were grafted beneath the right renal capsules of hypophysectomized-ovariectomized adult hamster hosts with a catheter implanted in the external jugular vein. After treatment, hosts were decapitated and graft tissue was stained for FSH and LH immunoreactivity. The mean percentage of adenohypophysial cells that stained for FSH was low (2.8%) in grafts in hosts infused continuously with heparinized saline vehicle for 7 days. In other hosts, peptides were pulsed through the catheter every 12 h for 7 days. The mean percentage of FSH cells also was low after pulsing 6 ng LHRH or 2 micrograms NPY but increased substantially when the two peptides were pulsed simultaneously. No differences in the mean percentage of LH cells existed between any of the groups. The results demonstrate that NPY and LHRH can synergize to induce cellular FSH immunoreactivity in the neonatal female hamster.

Animals↗

PubMed1994

Changes in pulsatile release of neuropeptide-Y and luteinizing hormone (LH)-releasing hormone during the progesterone-induced LH surge in rhesus monkeys.

In previous studies we have shown that the pulsatility of LH-releasing hormone (LHRH) release in gonadectomized monkeys is modulated by input from neuropeptide-Y (NPY) neurons: 1) the endogenous release of NPY in the stalk-median eminence (S-ME) was pulsatile; 2) NPY pulses were temporally correlated with LHRH pulses, with NPY pulses preceding LHRH pulses by approximately 5 min; and 3) infusion of NPY into the S-ME stimulated LHRH release, whereas 4) infusion of antiserum to NPY suppressed endogenous LHRH pulses. It is not known, however, whether ovarian steroid hormones alter the pulsatility of NPY and LHRH release or whether the temporal correlation of NPY and LHRH pulses is maintained during the LH surge. In the present study we examined the changes in pulsatile release of NPY and LHRH in ovariectomized monkeys treated with estradiol benzoate (EB) followed by progesterone or oil. Using push-pull perfusion, perfusate samples from S-ME were collected at 10-min intervals for 15 h. NPY and LHRH concentrations in the perfusates were measured by RIA. Circulating LH levels were also monitored by periodic blood sampling and RIA. Injection of progesterone (sc) after EB induced an LH surge with a peak latency of 7.3 +/- 1.3 h (mean +/- SE) in seven of seven monkeys, whereas oil injection after EB elicited an LH surge in none of seven monkeys. The progesterone-induced LH surge was associated with an increase in LHRH release; the mean, pulse amplitude, and pulse frequency increased significantly (for all, P < 0.05) 4-8 h after progesterone. NPY pulse frequency also increased significantly (P < 0.05) 4-8 h after progesterone treatment, whereas mean release and pulse amplitude did not change in response to progesterone. Oil treatment after EB administration did not alter any parameter of LHRH and NPY pulses. Interestingly, the NPY and LHRH pulses were highly correlated (P < 0.001) in monkeys treated with either EB-progesterone or EB-oil, and NPY pulses preceded LHRH pulses by 4.8 +/- 0.7 and 5.1 +/- 0.6 min, respectively. In summary, 1) an episode of increased LHRH release occurs before and during the progesterone-induced LH surge; 2) acceleration of LHRH pulse frequency and the increase in LHRH pulse amplitude after progesterone are accompanied by acceleration of NPY pulse frequency; and 3) ovarian steroids do not affect the temporal correlation between NPY and LHRH pulses.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1993

Estrogen alters the effects of neuropeptide-Y on luteinizing hormone and follicle-stimulating hormone release in female rats at the level of the anterior pituitary gland.

In recent years, several studies have shown that neuropeptide-Y (NPY) is involved in the control of LH secretion. We determined the effects of estrogen on NPY-induced LH and FSH release in the absence or presence of LH-releasing hormone (LHRH) at the level of the anterior pituitary gland (APG). Adult female rats were ovariectomized. Fifteen to 20 days later, they were given a blank or estrogen-filled capsule subdermally and killed 17-19 h later. APG cells were isolated and cultured for 3 days in medium containing 12.5% rat serum collected at death from the same rats used to make the respective APG cell pools. The cells were then challenged for 3 h with vehicle, NPY (10(-12)-10(-6) M), LHRH (10(-9)-10(-6) M), or combinations of NPY (10(-9)-10(-7) M) and LHRH (10(-9) M). LHRH stimulated LH and FSH release from nonestrogen and estrogen-primed cells. NPY at 6.7 x 10(-8)-10(-6) M increased (P < 0.05) LH release and at 10(-6) M increased (P < 0.05) FSH release from estrogen-primed cells, but was without effect on nonestrogen-primed cells. In contrast, NPY at 10(-9)-10(-7) M potentiated the action of LHRH (10(-9) M) to increase the release of LH and FSH from nonestrogen-primed cells, but was without potentiating effects in cultures of estrogen-primed cells. The results demonstrate that 1) NPY can release LH and FSH by a direct action on estrogen-primed APG cells; and 2) NPY can potentiate the action of LHRH to increase the release of LH and FSH by a direct action on nonestrogen-primed APG cells.

Animals↗

PubMed1992

Estradiol enhances the action of neuropeptide Y on in vivo luteinizing hormone-releasing hormone release in the ovariectomized rhesus monkey.

The effect of estrogen on the responsiveness of the luteinizing hormone-releasing hormone (LHRH) neurosecretory system to neuropeptide Y (NPY) stimulation was examined using a push-pull perfusion method in conscious monkeys. NPY, at doses of 10(-6) to 10(-12) M, was infused into the stalk-median eminence (S-ME) of ovariectomized monkeys with or without estrogen, while perfusates were continuously collected. LHRH in perfusates was measured by RIA. The results indicate that in both estrogen-primed and unprimed monkeys, NPY infusion into the S-ME elicited LHRH release in a dose-dependent manner (p < 0.01). Moreover, estrogen priming enhanced the responsiveness of LHRH release to NPY infusion: (1) the minimum NPY dose necessary to elicit a significant LHRH response was reduced, (2) the peak LHRH response to NPY at a dose of 10(-6) to 10(-10) M was increased, and (3) the total release of LHRH in response to NPY at doses of 10(-6) to 10(-12) M was increased. These results suggest that NPY stimulates LHRH release in the S-ME in the presence or absence of estrogen and that estrogen enhances the responsiveness of the LHRH neurosecretory system to NPY stimulation in the rhesus monkey.

Animals↗

PubMed1992

Neuropeptide Y is a neuromodulator of pulsatile luteinizing hormone-releasing hormone release in the gonadectomized rhesus monkey.

In a previous study, we have demonstrated that infusion of neuropeptide Y (NPY) into the stalk-median eminence (S-ME) of gonadectomized rhesus monkeys stimulated LHRH in a dose-dependent manner. This finding led us to address the following questions: 1) What are the characteristics of NPY release in vivo? 2) How does NPY release relate to LHRH release? 3) Is endogenous NPY essential to pulsatile LHRH release? To answer these questions, three experiments using push-pull perfusion were performed in adult gonadectomized rhesus monkeys. Perfusate samples from the S-ME were collected at 10-min intervals for 6 to 12-h periods, and the concentrations of LHRH and NPY in perfusates were determined by RIA. In Exp I, the release pattern of NPY and LHRH in the S-ME was independently determined in a group of 11 conscious monkeys: NPY release in the S-ME was pulsatile with an interpulse interval of 44.9 +/- 3.3 min (n = 11). This interpulse interval was similar to that seen for LHRH release (43.8 +/- 1.1 min, n = 7). Exp II was designed to determine whether NPY pulses and LHRH pulses occur synchronously and to examine whether NPY release in the S-ME is correlated with circulating LH pulses. NPY and LHRH concentrations in aliquots of the same perfusate sample from the S-ME and circulating LH levels were concurrently measured in 8 monkeys sedated with Saffan. It was found that NPY pulses were temporally correlated (P less than 0.001) with LHRH pulses, which were also temporally correlated (P less than 0.001) with LH pulses. Moreover, NPY pulses were correlated (P less than 0.05) with LH pulses. NPY peaks preceded LHRH peaks by 4.5 +/- 0.6 min, LHRH peaks preceded LH peaks by 5.5 +/- 0.6 min, and NPY peaks preceded LH peaks by 9.7 +/- 0.8 min. In Exp III, the role of endogenous NPY in LHRH release was evaluated by infusing a specific antiserum to NPY into the S-ME during push-pull perfusion in 8 conscious monkeys. Infusion of a specific antiserum to NPY into the S-ME at 1:100 and 1:1000 dilutions suppressed pulsatile LHRH release significantly (P less than 0.05). Infusion of nonimmune serum as a control was without effect. These results are summarized as follows: 1) NPY release in the S-ME is pulsatile, 2) NPY pulses occur synchronously with LHRH and LH pulses, and 3) immunoneutralization of endogenous NPY in the S-ME suppresses pulsatile LHRH release.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1991

Infusion of neuropeptide Y into the stalk-median eminence stimulates in vivo release of luteinizing hormone-release hormone in gonadectomized rhesus monkeys.

Studies in the rat and rabbit indicate that facilitatory effects of neuropeptide Y (NPY) as well as norepinephrine (NE) on LH and LHRH release are dependent on the presence of the ovarian steroid estrogen. However, we have previously found the NE and an alpha-1-adrenergic agonist are both stimulatory to pulsatile LHRH release in ovariectomized rhesus monkeys. In the present experiment the effects of NPY on LHRH release were examined in conscious monkeys using a push-pull perfusion method. Twelve gonadectomized monkeys (8 females and 4 males) were used. Perfusate samples from the stalk-median eminence (S-ME) were obtained through a push-pull cannula at 10-min intervals for 12 h, and the amount of LHRH in samples were determined with RIA. NPY dissolved in a modified Krebs-Ringer phosphate buffer solution at concentrations of 10(-8), 10(-7), 10(-6), and 10(-5) M was directly infused into the S-ME through the push cannula for 10 min at 90-min intervals. Vehicle was infused as a control. Since sex differences in LHRH response to NPY were not present, data from males and females were combined for analysis. NPY infusion into the S-ME stimulated LHRH release in a dose-dependent manner (P less than 0.001). The peak LHRH responses (mean +/- SEM) to NPY at different concentrations were: 10(-8) M = 2.1 +/- 0.4 pg/ml; 10(-7) M = 2.6 +/- 0.5 pg/ml; 10(-6) M = 6.5 +/- 1.1 pg/ml; 10(-5) M = 15.1 +/- 2.9 pg/ml, whereas to vehicle 0.37 +/- 0.17 pg/ml. All NPY doses tested were significantly effective as compared to vehicle (P less than 0.01). The LHRH response to 10(-6) M was greater (P less than 0.01) than that of 10(-8) M or 10(-7) M, and the response to 10(-5) M was greater (P less than 0.01) than that of all lower doses. The results indicate that NPY infusion into the S-ME elicits the release of LHRH in vivo in a dose-dependent manner in the monkey. The data further suggest that LHRH neurons and/or neuroterminals in the monkey are responsive to NPY stimulation in the absence of gonadal steroids. It is concluded that in addition to NE, NPY is an important regulator of pulsatile LHRH release in the nonhuman primate.

Animals↗

PubMed1988

The role of arginine vasotocin and prostaglandin F2 alpha on oviposition and luteolysis in the common snapping turtle Chelydra serpentina.

The administration of arginine vasotocin (AVT) to gravid snapping turtles with steroidogenically active corpora lutea and high plasma progesterone concentration (1480 +/- 155 pg/ml) did not trigger oviposition, whereas 12 days after ovulation when luteolysis occurred and plasma progesterone concentration was low (570 +/- 78 pg/ml), treatment with AVT caused oviposition. Controls with high plasma progesterone concentration (1605 +/- 185 pg/ml) oviposited 15-23 days after ovulation when plasma progesterone concentration dropped to 201 +/- 35 pg/ml. Deluteinization-induced oviposition was initiated 15 hr after surgery and was completed by 30 hr. Oviposition of complete clutches occurred and was correlated with a significant drop in plasma progesterone. Sham-operated turtles did not exhibit oviposition and no significant change in progesterone concentration was observed. A single injection of prostaglandin F2 alpha (PGF) in recently ovulated turtles induced early luteolysis and a significant decrease in plasma progesterone concentration after 24-30 hr. A single administration of PGF caused the disappearance of steroidogenic features such as the smooth endoplasmic reticulum and mitochondria with tubular cristae 48 hr later. Also PGF triggered the invasion of a hyaline-like material from the luteal theca into the luteal cell mass which eventually induced luteolysis. The role of AVT, PGF, and progesterone in relation to egg retention and oviposition is discussed.

Animals↗

PubMed1986

Lyophilized airborne Clostridium botulinum spores as inocula that intestinally colonize antimicrobially pretreated adult mice.

Adult mice, made susceptible to Clostridium botulinum by feedings of metronidazole, were immobilized with an anesthetic and held for 30 min in isolators in which a fine powder of lyophilized pathogen spores was made airborne. Exposed mice were surface decontaminated before being kept for 2 days in holding isolators. Mice were intestinally colonized by the pathogen. Colonization rates were related to spore numbers (10(4) to 10(7) type A or B) seeded into isolators.

Aerosols↗

PubMed1986

Cytoplasmic progesterone receptors in uterine tissue of the snapping turtle (Chelydra serpentina).

A high affinity progesterone-binding component was detected in the cytosol of the uterus of the snapping turtle, Chelydra serpentina. Density gradient centrifugation indicated that binding of [3H]progesterone and [3H]promegestone (R5020) was to a fraction with a heavier sedimentation coefficient than bovine serum albumin (BSA) appearing as a broader peak in the 6-7 S region; it was not affected by excess cortisol. Another binding peak, lighter than BSA and appearing with [3H]R5020 and [3H]progesterone near the 4 S region, was affected by excess cortisol. Excess progesterone decreased both the heavier and lighter peaks. Analysis of steroid specificity revealed that, of the natural steroids, progesterone had the highest affinity for the uterine cytosol. This was followed by deoxycorticosterone, 5 alpha-pregnanedione, testosterone, oestradiol-17 beta, corticosterone, 5 alpha-dihydrotestosterone and cortisol. Non-linear regression analysis of saturation data indicated the presence of two classes of high affinity binding sites: progesterone-binding sites (R-sites) with equilibrium association constants (Ka) of 2.9 +/- 0.28 litres/nmol (mean +/- 95% confidence limit) for [3H]R5020 and 0.34 +/- 0.20 litres/nmol for [3H]progesterone, and corticosteroid-binding globulin-like sites (G-sites) with Ka of 4.5 +/- 1.6 litres/nmol for progesterone. The concentration of R-sites was between 0.66 +/- 0.10 and 2.6 +/- 0.55 pmol/mg protein while that of G-sites was between 0.73 +/- 0.05 and 5.0 +/- 0.27 pmol/mg protein. DEAE-cellulose filtration assay also confirmed the presence of R-sites and G-sites in the cytosol. R-sites were detectable without oestrogen priming during the preovulatory and vitellogenic phases (low progesterone, high oestrogen concentrations) when the ovarian follicles are mature (18-22 mm diameter).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Ultrastructural changes in testes of the snapping turtle, Chelydra serpentina in relation to plasma testosterone, delta 5-3 beta-hydroxysteroid dehydrogenase, and cholesterol.

Ultrastructural changes in the testes of the common snapping turtle, Chelydra serpentina, were observed throughout the year. Plasma testosterone levels were measured and compared with the occurrence of delta 5-3 beta-hydroxysteroid dehydrogenase (3 beta-HSD), cholesterol, and steroidogenic ultrastructural features (smooth endoplasmic reticulum (SER), mitochondria with tubular cristae) in Sertoli and Leydig cells. The testosterone level is highest in May and October (mating) and relatively low during the rest of the year. Fluctuations in 3 beta-HSD and cholesterol are consistent with the interpretation that the Leydig cells are potentially active throughout the year. They undergo very little ultrastructural change, (tubular SER to vesiculate and loss of golgi during spermatogenesis and in the winter). Sertoli cells are active only during spermatogenesis from May through October and become inactive until the next cycle; 3 beta-HSD, cholesterol and ultrastructural features change more drastically in the Sertoli cells than in the Leydig cells. These results are discussed with reference to the hypothesis that testosterone of Leydig origin is concerned mainly with mating behavior and that of Sertoli origin with spermatogenesis and maturation of sperm.

3-Hydroxysteroid Dehydrogenases↗

PubMed1985

Development of the ovarian follicles in relation to changes in plasma parameters and 5 delta 3 beta HSD in snapping turtle, Chelydra serpentina.

Follicular development in snapping turtle, Chelydra serpentina, was studied in relation to changes in plasma levels of estradiol-17 beta, total protein, calcium, inorganic phosphate and cholesterol. Histochemical reaction for 3 beta-HSD in granulosa and theca cells of the follicles is strong during the preovulatory and vitellogenic phases when the follicles attain their maximum size (18-22 mm) and estradiol is at a high level. The reaction for 3 beta-HSD is weal during the postovulatory phase when the developing follicles are at their minimum size (5-7 mm) and estradiol is low. Administration of estradiol-17 beta causes a rise in plasma calcium, total protein, inorganic phosphate and cholesterol.

3-Hydroxysteroid Dehydrogenases↗