| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
RESEARCH |
1 Animal Reproduction Laboratory, Texas A&M University Agricultural Research Station, Beeville, Texas 78102, USA, 2 Department of Animal Science and 3 Center for Animal Biotechnology and Genomics, Texas A&M University, College Station, Texas 77843, USA, 4 Department of Animal and Wildlife Sciences, Texas A&M University-Kingsville, Kingsville, Texas 78363 USA and 5 Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana 70808, USA
Correspondence should be addressed to G L Williams; Email: glw{at}fnbnet.net
 |
Abstract |
|---|
 Top Abstract IntroductionMaterials and MethodsResultsDiscussionAcknowledgementsReferences |
|---|
|
Introduction |
|---|
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionAcknowledgementsReferences |
|---|
In addition to the roles of GnRH and gonadal hormones in controlling the secretion of FSH, the existence of a separate, highly specific FSH-releasing hormone (FSH-RH) of hypothalamic origin has been proposed. Experimental evidence to support this theory has included the identification of separate fractions of FSH-RH and LH-releasing hormone activity in sheep hypothalamic extracts (Dhariwal et al. 1965), as well as selectively impaired release of FSH after lesioning of the dorsal anterior hypothalamic area (Lumpkin & McCann 1984) and posterior/-mid infundibulum (Marubayashi et al. 1999). Moreover, GnRH-independent pulses of FSH have been detected by determining concentrations of FSH in the hypothalamic–hypophyseal portal circulation (Padmanabhan et al. 2003).
Biochemically, several alternative forms of GnRH have been identified in vertebrates (Dubois et al. 2002) and have been examined as candidates for selective FSH-RH activity. One of these, identical to chicken GnRH-II, and its receptor have been identified in mammals (Lescheid et al. 1997, Millar et al. 2001). Although not isolated in mammals to date, an alternative form of GnRH, lamprey GnRH-III (lGnRH-III) (Sower et al. 1993), has been reported to selectively stimulate the release of FSH in rodents (Yu et al. 1997) and in cattle during the luteal phase of the estrous cycle (Dees et al. 2001). However, several other studies, both in vitro (Yu et al. 1997, Lovas et al. 1998, Montaner et al. 2001, Kovacs et al. 2002) and in vivo (Kovacs et al. 2002), have questioned the ability of lGnRH-III to selectively release FSH in rodents. Clearly, the existence of a distinct mammalian FSH-RH could have far-reaching implications in both medicine and agriculture. Therefore, the objectives of studies reported herein were to assess the ability of lGnRH-III to preferentially release FSH in an array of physiological contexts in cattle.
|
Materials and Methods |
|---|
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionAcknowledgementsReferences |
|---|
Synthesis of lGnRH-III
lGnRH-III was synthesized by the Protein Facility at Louisiana State University. The peptide was found to be 100% pure by HPLC and exhibited a mass spectrophotometric peak of 1259.5 (molecular mass of lGnRH-III is 1259 Da).
Experiment 1: effects of lGnRH-III in primary adenohypophyseal cell cultures
Hypophyses were collected from steers at slaughter at the Rosenthal Meat Science Center, Texas A&M University, College Station, Texas and kept on ice until tissue processing. Adenohypophyses were dissected from the neurohypophysis and adenohypophyseal cells were dispersed enzymatically as described previously (Welsh et al. 1986, Tanner et al. 1990). Dispersed cells from two steers were combined, plated in six-well plates, and cultured in Dulbecco’s modified Eagle’s medium (DMEM) containing 10% fetal calf serum for 4 days. On day 4, cells were incubated with serum-free DMEM overnight. On the next day, cells were treated with DMEM alone (control), DMEM containing 10-6, 10-7, 10-8 or 10-9 M mammalian GnRH-I (mGnRH) (Bachem Inc., Torrance, CA, USA) or DMEM containing lGnRH-III at the same concentrations as mGnRH for 4 h. Each treatment was applied to six wells. At the end of the 4 h incubation, culture media were harvested, and stored at -20 °C until assayed for LH and FSH. Three independent replications were performed.
Experiment 2: effects of lGnRH-III in ovariectomized cows with basal circulating concentrations of estradiol
Seven ovariectomized cows, each bearing a Silastic (Dow Corning Corporation, Midland, MI, USA) ear implant containing crystalline estradiol 17-ß (Sigma, St Louis, MO, USA), were used. This animal model has been used extensively to study the neuroendocrine control of gonadotropin secretion in cattle without the complications associated with ovarian cyclicity. In this experiment, implants provided mean concentrations (±S.E.M.) of estradiol of 5.46 ± 0.16 pg/ml. Cows were injected i.v. with (i) physiological saline (control), (ii) mGnRH in saline (0.055, 0.11 and 0.165 µg/kg body weight (BW), and (iii) lGnRH-III (same doses as mGnRH) in a Latin Square design, such that each cow received one of the treatments in random order on each day of a 7 day experiment. Therefore, each treatment was applied only once to each experimental cow and no more than one treatment was applied to each cow on a given day. Blood was collected by venipuncture immediately prior to treatment (time 0) and at 10, 30, 60, 120 and 240 min after injections.
Experiment 3: effects of lGnRH-III in the presence of basal estradiol and mid-luteal phase levels of progesterone
Five ovariectomized cows, each bearing estradiol implants similar to those described in Experiment 2, were used. Cows had mean (±S.E.M.) concentrations of estradiol of 4.88 ± 0.19 pg/ml. To mimic luteal-phase concentrations of progesterone, cows received a single controlled release drug delivery device (CIDR) (Pharmacia Animal Health, Kalamazoo, MI, USA) intravaginally 2 days before the experiment began. CIDR devices were left in place for the duration of the experiment. In addition, i.m. injections of 100 mg progesterone (Sigma) diluted in vegetable oil were administered daily. Injections of progesterone started on the day before the experiment began and continued for the duration of the study, producing mean (±S.E.M.) concentrations of progesterone of 8.8 ± 0.5 ng/ml. Cows were treated i.v. with (i) saline (control), (ii) mGnRH in saline (0.11 or 1.1 µg/kg BW), and (iii) lGnRH-III in saline (same doses as for mGnRH) in a Latin Square design (i.e. each cow received one treatment in random order on each day of the 5 day experiment as in Experiment 2). Therefore, each treatment was applied only once to each experimental cow and no more than one treatment was applied to each cow on a given day. Blood was collected by venipuncture immediately prior to treatment (time 0) and at 10, 30, 60, 120 and 240 min after injections.
Experiment 4: effects of lGnRH-III during the mid-luteal phase of the estrous cycle
Experiment 4A
Estrous cycles were synchronized in six cows using a 7 day treatment with CIDR devices and an injection of a synthetic prostaglandin analog, dinoprost tromethamine (Lutalyse; Pharmacia Animal Health, Kalamazoo, MI, USA) on the day of CIDR removal. On day 10, 11 or 12 after estrus, cows were injected i.v. with (i) saline (control), (ii) mGnRH in saline (1.1 µg/kg BW), and (iii) lGnRH-III (1.1 µg/kg BW) in two replicates with three cows per replicate. As in Experiments 2 and 3, releasing hormone treatments or saline were administered in a Latin Square design in a 3 day experiment and no more than one treatment was applied to each cow on a given day. Blood was collected by venipuncture immediately prior to treatment (time 0) and at 10, 30, 60, 120 and 240 min after injections. Mean concentrations (±S.E.M.) of progesterone observed during this experiment were 4.2 ± 0.25 ng/ml.
Experiment 4B
Because of an apparent change in sensitivity to lGnRH-III in mid-luteal phase cows in Experiment 4A (see Results) compared with ovariectomized cows (Experiments 2 and 3), higher doses of lGnRH-III were tested in this experiment. Three intact cows with estrous cycles synchronized using a single injection of Lutalyse administered during the mid-luteal phase were used. Cows were injected i.v. with (i) saline (control) or (ii) lGnRH-III in saline (1.1 or 4.4 µg/kg BW). Injections were administered in a Latin Square design in a 3 day experiment and no more than one treatment was applied to each cow on a given day, as in previous experiments. Because synchronization of estrus using only a prostaglandin can result in a wide distribution in time of onset of estrus compared with other methods, the stage of follicular development at the time of corpus luteum regression (Bó et al. 2002) could potentially influence the regulation of FSH. To minimize these effects, two cows were used on days 10–12 and one cow was used on days 11–13 after estrus. Blood was collected by venipuncture immediately prior to treatment (time 0) and at 10, 30, 60, 120 and 240 min after injections. Mean concentrations (±S.E.M.) of progesterone observed during the experiment were 4.5 ± 0.41 ng/ml.
RIAs
Concentrations of LH in culture media collected from each well (Experiment 1) and in serum (Experiments 2–4) were determined with a validated RIA as described previously (McVey & Williams 1991). Intra- and interassay coefficients of variation averaged 5.9 and 10.6% respectively. Concentrations of FSH in culture media (Experiment 1) and serum (Experiments 2–4) were determined using an RIA described previously by Krystek et al. (1985). In this assay, a highly purified ovine FSH (oFSH) (AFP 5679C; National Hormone and Pituitary Program (NHPP), Harbor-UCLA Medical Center, Torrance, CA, USA) was used as both the reference preparation and as iodinated tracer. Antiserum produced in rabbits immunized against oFSH was utilized as the primary antiserum. This antiserum shows similar cross-reactivity between partially purified preparations of oFSH (oFSH S8 and S9; NHPP) and bovine FSH (bFSH B1; NHPP) and does not cross-react with other pituitary hormones (Krystek et al. 1985). Sensitivity of the assay averaged 0.05 ng/ml. Intra- and interassay coefficients of variation averaged 5.7 and 9.6% respectively.
Because of the heterogeneity of FSH molecules (Padmanabhan et al. 1992) and varied sources of reference hormones, iodinated tracers and antiserum in RIAs for ruminant FSH, the above RIA plus two additional FSH assay systems were compared in Experiment 3. Assay 2, referred to hereafter as the Bolt assay, used a bFSH preparation (AFP 5332B; NHPP) as both the reference preparation and as iodinated tracer (Bolt & Rollins 1983). The antiserum (US Department of Agriculture (USDA) 5-0122) utilized in this assay was raised against bFSH-ß and reacts with intact molecules of FSH, but does not react significantly with the 
-subunit of bFSH or other pituitary hormones (Bolt & Rollins 1983). Sensitivity of the single assay performed was 0.05 ng/ml. The intra-assay coefficient of variation averaged 7.2%. The third RIA system utilized highly purified bFSH (AFP-5332B; NHPP) as the reference preparation and iodinated tracer. The antiserum (AFP7711690; NHPP) was raised against intact bFSH. Sensitivity of the single assay performed was 0.06 ng/ml. The intra-assay coefficient of variation averaged 5.6%.
Serum concentrations of estradiol were determined in extracted samples in a single assay as reported previously (Talavera et al. 1985). Concentrations of progesterone were determined in selected samples in a single assay with the Coat-A-Count direct assay (Diagnostic Products, Los Angeles, CA, USA) as reported previously from this laboratory (Fajersson et al. 1999). Sensitivity for estradiol and progesterone assays was 3.7 pg/ml and 0.05 ng/ml respectively. The intra-assay coefficients of variation for these assays averaged 2.7 and 4.2% respectively.
Statistical analysis
In Experiment 1, LH and FSH data were analyzed by ANOVA using the general linear models procedure (PROC GLM) of the Statistical Analysis System (SAS 8.1; SAS Institute Inc., Cary, NC, USA). Sources of variation were treatment, well(treatment), replication, and treatment x replication interaction. A significant replicate effect was observed; thus, treatment effects were analyzed for each replication. The least significant difference was used to compare means when significant differences were detected by ANOVA.
In Experiments 2–4, LH and FSH data were analyzed by ANOVA using the PROC GLM procedure of SAS for a Latin Squares design. Sources of variation were cow, day and treatment. The least squares means procedure was used to compare means when significant differences were detected. Adenohypophyseal responses in each experiment were also analyzed by examining maximum (peak) release and areas under the response curves for LH and FSH. Because results of these analyses resulted in identical interpretations to those obtained with the ANOVA of mean concentrations following releasing hormone challenges, only the results of the latter analyses are presented in the Results.
|
Results |
|---|
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionAcknowledgementsReferences |
|---|
.
|
).
|
). However, only the highest dose of lGnRH-III (1.1 µg/kg) stimulated (P < 0.001) a non-selective release of both LH and FSH (Fig. 3). A comparison of three FSH RIA systems, widely available for use by other investigators, produced comparable results and demonstrated that the higher dose of lGnRH-III induced (P < 0.005) a non-selective release of FSH (Fig. 4). No stimulation of release of FSH was observed with the lower dose.
|
|
). As expected, mGnRH at the same dose (1.1 µg/kg) released (P < 0.001) both LH and FSH (Fig. 5).
|
). Similar to experiment 4A, a dose of 1.1 µg/kg lGnRH-III did not stimulate the release of either LH or FSH (Fig. 6).
|
|
Discussion |
|---|
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionAcknowledgementsReferences |
|---|
The amino acid sequence of lGnRH-III exhibits a 60% homology to that of mGnRH (type I). The two molecules differ in sequence at amino acid positions 5–8, which confers distinct conformational characteristics that may account for differences in biological activity (Watts et al. 2001). Yu et al. (2000) reported selective FSH-releasing activity in fractions of gel-purified hypothalamic extracts that could be neutralized by antisera against lGnRH and proposed that the putative FSH-RH fractions were lGnRH-III or a closely related peptide. However, Montaner et al. (2001) were unable to detect selective FSH-releasing activity in rat and hamster hypothalamic extracts purified by HPLC. At least two other reports have failed to demonstrate selective FSH release by lGnRH-III in rat pituitary cells (Lovas et al. 1998, Montaner et al. 2001).
In the present study, we observed that lGnRH-III induced gonadotropin release from bovine primary adenohypophyseal cells at concentrations of 10-7 and 10-6 M, but not at lower concentrations. Importantly, there was no selective release of FSH by lGnRH-III, similar to that reported by Yu et al. (2002) in primary rat adenohypophyseal cells. Therefore, there is general agreement among studies that, in primary cultures of adenohypophyseal cells, lGnRH-III does not stimulate the release of gonadotropins at low concentrations, but at higher concentrations it stimulates a non-selective release of both LH and FSH. In contrast, in vitro studies using hemipituitaries suggested that lGnRH-III could preferentially release FSH (Yu et al. 1997, 2002). Whether the divergent effects of lGnRH-III in primary adenohypophyseal cell cultures vs hemipituitaries were due to differences in the physiological state of gonadotropes is not clear. Yu et al. (2002) proposed that the lack of selective responsiveness of cultured adenohypophyseal cells to lGnRH-III is due to the absence of gonadal steroids, resulting in a down-regulation of putative lGnRH-III receptors.
Because reports on in vivo studies testing the effects of lGnRH-III on gonadotropin secretion have been inconsistent, a careful examination of lGnRH-III action during different physiological/endocrinological states and at different doses seems prudent. Dees et al. (2001) reported that doses of 0.25 and 0.5 mg lGnRH-III selectively stimulated the release of FSH during the luteal phase (days 9–14) of the estrous cycle in cows. However, doses of 2 or 8 mg lGnRH-III released both LH and FSH during this period. In contrast, 0.5 mg lGnRH-III released only LH during the follicular phase of the estrous cycle and was less potent in this effect than mGnRH (Dees et al. 2001). These findings are interpreted to mean that low doses of lGnRH-III have the ability to selectively stimulate FSH release during periods of high circulating progesterone. The report did not discuss how this occurs in the face of expected increases in circulating inhibin that are associated with the development of second-wave follicle dominance during this time period (see review by Padmanabhan et al. 2002).
In our experiments using the ovariectomized, estradiol-implanted cow without any progesterone treatment, doses of lGnRH-III of up to 0.165 µg/kg (equivalent to ~0.075 mg) failed to elicit measurable release of either gonadotropin. In contrast, doses of mGnRH as low as 0.055 µg/kg (equivalent to ~0.025 mg) effectively released both LH and FSH. Using the ovariectomized, estradiol-implanted cow, with exogenous progesterone treatment to simulate luteal-phase concentrations of progesterone, we observed that doses of 1.1 µg/kg (equivalent to ±0.5 mg) lGnRH-III stimulated a non-selective release of both LH and FSH. Thus, similarly to the studies reported by Kovac et al. (2002) using the ovariectomized, estradiol/progesterone-treated rat, lGnRH-III did not stimulate preferential release of FSH in our studies with cattle. Moreover, during the mid-luteal phase (days 10–12) in the intact cow, doses of 1.1 µg/kg lGnRH-III failed to release either LH or FSH. However, doses of 4.4 µg/kg (equivalent to ±2 mg) lGnRH-III released only LH. Therefore, the ability of lGnRH-III to stimulate the release of gonadotropins was impaired during this period. It is generally accepted that ovarian follicular inhibins and follistatins suppress FSH secretion (Padmanabhan et al. 2002) without apparent effects on secretion of LH (Rivier et al. 1986); nonetheless, a decrease in the number of binding sites for GnRH induced by inhibin has been reported (Wang et al. 1988). Thus, if lGnRH-III has lower binding affinity for GnRH receptors, potential decreases in numbers of GnRH receptors on gonadotropes induced by ovarian hormones could also account for significantly diminished responsiveness to lGnRH-III. lGnRH-III is also less potent compared with mGnRH (type I and II) for inducing inositol-phosphate production in COS-1 cells expressing GnRH receptors I and II (Neill 2002). Therefore, while it remains possible that lGnRH-III acts on a distinct receptor other than GnRH-I or -II, as proposed by Yu et al. (2000); no sequence for GnRH receptor forms, other than types I and II and a non-functional GnRH receptor-like homologue, has been observed in the human genome (Neill et al. 2001).
FSH molecules are largely heterogeneous and may vary in immunological and biological activities (Padmanabhan et al. 1992). To examine whether the discordant results obtained in our experiments and those performed by Dees et al. (2001), both involving cattle, could be accounted for by potential differences in immunological assay methodology, we used three distinct RIA systems validated for use in bovine samples. All three RIAs used to determine concentrations of FSH produced similar results. Therefore, it is not likely that contrasting observations between our experiments and those performed by Dees et al. (2001) are due to differences in the ability of particular RIAs used to detect circulating FSH.
In summary, results from our experiments do not provide evidence that lGnRH-III can selectively release FSH in cattle. The identification of such a factor would have important implications in both animal agriculture and human medicine.
|
Acknowledgements |
|---|
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionAcknowledgementsReferences |
|---|
|
Footnotes |
|---|
|
References |
|---|
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionAcknowledgementsReferences |
|---|
Bó GA, Baruselli PS, Moreno D, Cutaia L, Caccia M, Tríbulo R et al. 2002 The control of follicular wave development for self-appointed embryo transfer programs in cattle. Theriogenology 57 53–72.[CrossRef][ISI][Medline]
Bolt DJ & Rollins R 1983 Development and application of a radio-immunoassay for bovine follicle-stimulating hormone. Journal of Animal Science 56 146–154.
Clarke IJ, Cummins JT & de Kretser DM 1983 Pituitary gland function after disconnection from direct hypothalamic influences in the sheep. Neuroendocrinology 36 376–384.[ISI][Medline]
Dees WL, Dearth RK, Hooper RN, Brinsko SP, Romano JE, Rahe H et al. 2001 Lamprey gonadotropin-releasing hormone-III selectively releases follicle stimulating hormone in the bovine. Domestic Animal Endocrinology 20 279–288.[CrossRef][ISI][Medline]
Dhariwal APS, Nallar R, Batt M & McCann SM 1965 Separation of follicle-stimulating hormone-releasing factor from luteinizing hormone-releasing factor. Endocrinology 76 290–294.
Dubois EA, Zandbergen MA, Peute J & Goos HJ 2002 Evolutionary development of three gonadotropin-releasing hormone (GnRH) systems in vertebrates. Brain Research Bulletin 57 413–418.[CrossRef][ISI][Medline]
Fajersson P, Stanko RL & Williams GL 1999 Distribution and repeatability of anterior pituitary responses to GnRH and relationship of response classification to the postpartum anovulatory interval of beef cows. Journal of Animal Science 77 3043–3049.
Knobil E 1980 The neuroendocrine control of the menstrual cycle. Recent Progress in Hormone Research 36 53–88.
Kovacs M, Koppan M, Mezo I, Teplan I & Flerko B 1993 Antiovulatory doses of antagonists of LH-RH inhibit LH and progesterone but not FSH and estradiol release. Journal of Neuroendocrinology 5 603–608.[CrossRef][ISI][Medline]
Kovacs M, Seprodi J, Koppan M, Horvath JE, Vincze B, Teplan I et al. 2002 Lamprey gonadotropin hormone-releasing hormone-III has no selective follicle-stimulating hormone-releasing effect in rats. Journal of Neuroendocrinology 14 647–655.[CrossRef][ISI][Medline]
Krystek SR Jr, Dias JA, Reichert LE Jr & Andersen TT 1985 Prediction of antigenic sites in follicle-stimulating hormones: difference profiles enhance antigenicity prediction methods. Endocrinology 117 1125–1131.[Abstract]
Lescheid DW, Terasawa E, Abler LA, Urbanski HF, Warby CM, Millar RP et al. 1997 A second form of gonadotropin-releasing hormone (GnRH) with characteristics of chicken GnRH-II is present in the primate brain. Endocrinology 138 5618–5629.
Lovas S, Palyi I, Vincze B, Horvath J, Kovacs M, Mezo I et al. 1998 Direct anticancer activity of gonadotropin-releasing hormone-III. Journal of Peptide Research 52 384–389.[ISI][Medline]
Lumpkin MD & McCann SM 1984 Effect of destruction of the dorsal anterior hypothalamus on follicle-stimulating hormone secretion in the rat. Endocrinology 115 2473–2480.[Abstract]
Marubayashi U, Yu WH & McCann SM 1999 Median eminence lesions reveal separate hypothalamic control of pulsatile follicle-stimulating hormone and luteinizing hormone release. Proceedings of the Society for Experimental Biology and Medicine 220 139–146.[Abstract]
McVey WR Jr & Williams GL 1991 Mechanical masking of neurosensory pathways at the calf-teat interface: endocrine, reproductive, and lactational features of the suckled anestrous cow. Theriogenology 35 931–941.
Millar R, Lowe S, Conklin D, Pawson A, Maudsley S, Troskie B et al. 2001 A novel mammalian receptor for the evolutionarily conserved type II GnRH. PNAS 98 9636–9641.
Montaner AD, Mongiat L, Lux-Lantos VAR, Park MK, Fischer WH, Craig AG et al. 2001 Structure and biological activity of gonadotropin-releasing hormone isoforms isolated from rat and hamster brains. Neuroendocrinology 74 202–212.[CrossRef][ISI][Medline]
Neill JD 2002 GnRH and GnRH receptor genes in the human genome. Endocrinology 143 737–743.
Neill JD, Duck LW, Sellers JC & Musgrove LC 2001 A gonadotropin-releasing hormone (GnRH) receptor specific for GnRH II in primates. Biochemical and Biophysical Research Communications 282 1012–1018.[CrossRef][ISI][Medline]
Padmanabhan V, Mieher CD, Borondy M, I’Anson H, Wood RI, Landefeld TD et al. 1992 Circulating bioactive follicle-stimulating hormone and less acidic follicle-stimulating hormone isoforms increase during experimental induction of puberty in the female lamb. Endocrinology 131 213–220.[Abstract]
Padmanabhan V, Karsch FJ & Lee JS 2002 Hypothalamic, pituitary and gonadal regulation of FSH. Reproduction 59 (Suppl) 67–82.
Padmanabhan V, Brown MB, Dahl GE, Evans NP, Karsh FJ, Mauger DT, Neill JD & Cleeff JV 2003 Neuroendocrine control of follicle-stimulating hormone (FSH) secretion: III. Is there a gonadotropin-releasing hormone-independent component of episodic FSH secretion in ovariectomized and luteal phase ewes? Endocrinology 144 1380–1392.
Pau KY, Gliessman PM, Oyama T & Spies HG 1991 Disruption of GnRH pulses by anti-GnRH serum and phentolamine obliterates pulsatile LH but not FSH secretion in ovariectomized rabbits. Neuroendocrinology 53 382–391.[ISI][Medline]
Rivier C, Rivier J & Vale W 1986 Inhibin-mediated feedback control of follicle-stimulating hormone secretion in the female rat. Science 234 205–208.
Sower SA, Chiang Y, Lovas S & Conlon JM 1993 Primary structure and biological activity of a third gonadotropin-releasing hormone from lamprey brain. Endocrinology 132 1125–1131.[Abstract]
Talavera F, Park CS & Williams GL 1985 Relationships among dietary lipid intake, serum cholesterol, and ovarian function in Holstein heifers. Journal of Animal Science 60 1045–1051.
Tanner JW, Davis SK, McArthur NH, French JT & Welsh TH Jr 1990 Modulation of growth hormone (GH) secretion and GH mRNA levels by GH-releasing factor, somatostatin and secretagogues in cultured bovine adenohypophyseal cells. Journal of Endocrinology 125 109–115.[Abstract]
Wang QF, Farnworth PG, Findlay JK & Burger HG 1988 Effect of purified 31K bovine inhibin on the specific binding of gonadotropin-releasing hormone to rat anterior pituitary cells in culture. Endocrinology 123 2161–2166.[Abstract]
Watts CR, Mezei M, Murphy RF & Lovas S 2001 Conformational space comparison of GnRH and lGnRH-III using molecular dynamics, cluster analysis and Monte Carlo thermodynamic integration. Journal of Biomolecular Structure and Dynamics 18 733–748.
Welsh TH Jr, Harms PG, McArthur NH & Procknor M 1986 Regulation of adenohypophyseal hormones by hypothalamic neurohormones and activators of adenyl cyclase and protein kinase C. In Proceedings of 1st Membrane Protein Symposium, pp 703–713. Ed. S Goheen. San Diego, CA: Bio-Rad Laboratory Publishers.
Yu WH, Karanth S, Walczewska A, Sower SA & McCann SM 1997 A hypothalamic follicle-stimulating hormone-releasing decapeptide in the rat. PNAS 94 9499–9503.
Yu WH, Karanth S, Sower SA, Parlow AF & McCann SM 2000 The similarity of FSH-releasing factor to lamprey gonadotropin-releasing hormone III (l-GnRH-III). Proceedings of the Society for Experimental Biology and Medicine 224 87–92.
Yu WH, Karanth S, Mastronardi CA, Sealfon S, Dean C, Dees WL et al. 2002 Lamprey GnRH-III acts on its putative receptor via nitric oxide to release follicle-stimulating hormone specifically. Experimental Biology and Medicine 227 786–793.
This article has been cited by other articles:
 |
|
 |
|
  A. Bowen, S. Khan, L. Berghman, J. D. Kirby, R .P. Wettemann, and J. A. Vizcarra Immunization of pigs against chicken gonadotropin-releasing hormone-II and lamprey gonadotropin-releasing hormone-III: Effects on gonadotropin secretion and testicular function J Anim Sci, November 1, 2006; 84(11): 2990 - 2999. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
