Role of gonadal negative feedback on the gonadotrophin responses to gonadotrophin-releasing hormone (GnRH) in ram lambs from two lines of sheep selected for their luteinizing hormone response to GnRH.

Divergent selection has resulted in two lines of lambs (high and low) that have a 5-fold difference in their ability to release luteinizing hormone (LH) in response to 5 micrograms of gonadotrophin-releasing hormone (GnRH). Baseline gonadotrophin concentrations, the gonadotrophin responses to a GnRH challenge and the concentrations of testosterone and oestradiol were compared in lambs which were castrated at birth and intact lambs from both selection lines at 2, 6, 10 and 20 weeks of age. The pattern of LH and follicle-stimulating hormone (FSH) secretion was similar in the two lines, but differed between the intact and the castrated lambs. Basal LH and FSH secretion were significantly higher in the castrates than in the intact lambs from both selection lines. The high-line lambs had significantly higher basal FSH concentrations at all ages tested and significantly higher basal LH concentrations during the early postnatal period. The magnitude of the gonadotrophin responses to GnRH differed significantly between the intact and the castrated lambs within each line, the amount of gonadotrophins secreted by the castrated lambs being significantly greater. The removal of gonadal negative feedback by castration did not alter the between-line difference in either LH or the FSH response to the GnRH challenge. Throughout the experimental period, the concentration of testosterone in the intact lambs was significantly greater than in the castrated lambs in both selection lines, but no significant difference was seen in the concentrations of oestradiol. No significant between-line differences were found in the peripheral concentrations of testosterone or oestradiol in the intact lambs from the two selection lines. Therefore, despite similar amounts of gonadal negative feedback in the selection lines, there were significant between-line differences in basal gonadotrophin concentrations, at 2 and 6 weeks of age, and in the LH and FSH responses to an exogenous GnRH challenge, at all ages tested. Removal of gonadal negative feedback did not affect the magnitude of the between-line difference in the response of the lines to GnRH stimulation. The results indicate that the effects of selection on gonadotrophin secretion are primarily at the level of the hypothalamo-pituitary complex.     

Seasonal variation in hypothalamic content of gonadotropin-releasing hormone (GnRH), pituitary receptors for GnRH, and pituitary content of luteinizing hormone and follicle-stimulating hormone in the mare

Seasonal changes in the hypothalamic-hypophyseal axis were investigated using tissue from 49 light-horse mares, of mixed breeding. Hypothalamic and pituitary tissues were collected at 5 intervals throughout the years 1981 and 1982, representing midbreeding season (July, n = 10), transition out of the breeding season (October, n = 11), midanestrus (December, n = 8), transition into the breeding season (March, n = 10), and again in the following midbreeding season (July, n = 10). The hypothalamic region was dissected into preoptic area, body and median eminence. Gonadotropin-releasing hormone (GnRH) was extracted from hypothalamic samples with methanol-formic acid and quantified by radioimmunoassay. The anterior pituitary was homogenized and receptors for GnRH were quantified in a crude membrane fraction. Concentrations of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured in the resulting supernatant. Content of GnRH in each of the 3 hypothalamic areas varied with season (P less than 0.01) and was lowest during midanestrus (P less than 0.05). There was no effect of season (P greater than 0.01) on either concentration or total number of receptors for GnRH, or concentration of FSH in the anterior pituitary. Concentrations of LH in the anterior pituitary varied with season (P less than 0.001). Means (+/- SEM) for the 5 collection times were 15.5 +/- 2.7, 9.7 +/- 2.4, 2.3 +/- 0.5, 2.7 +/- 0.4 and 11.7 +/- 1.5 microgram LH/mg anterior pituitary, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Lack of gonadotrophin-releasing hormone (GnRH) neuron response to decreasing photoperiod in thyroidectomized male starlings (Sturnus vulgaris)

Exposure of starlings to long days initially causes reproductive maturation, but eventually leads to photorefractoriness. During photorefractoriness, gonadotrophin-releasing hormone (GnRH) decreases in the GnRH cell bodies and fibers emanating from these to the median eminence, circulating gonadotrophin concentrations decrease to a minimum, and the gonads regress. Thyroidectomy profoundly affects these photoperiodic responses. In chronically thyroidectomized starlings, gonadal responses to changes in day length are attenuated. This investigation was conducted to determine whether, in the absence of gonadal responsiveness, the GnRH system of chronically thyroidectomized starlings responds to changes in day length. Two groups of thyroidectomized male starlings were transferred from short days (8L:16D) to long days (18L:6D) for four weeks, and testicular volume increased. One group was kept on long days (TxLD) and the other was returned to short days (TxSD). Testicular volume did not decrease in the TxSD group. The GnRH neurons of the two thyroidectomized groups were compared to those of two groups of intact starlings, one of them on long days and photorefractory (ILD), the other on short days and photosensitive (ISD). Group ILD had lower numbers of GnRH-stained cells than groups TxLD, TxSD and ISD, which did not differ in this respect. Similar differences were observed for GnRH cell size in the pre-optic area (POA) and for density of staining of GnRH fibers in the median eminence. The results confirm that thyroidectomy attenuates gonadal responses to change in day length and suggest that this results from an effect upon the central nervous system rather than a peripheral effect.     

Identification of luteinizing hormone-releasing hormone (LH-RH) in the brain and pituitary gland of a fish by immunocytochemistry.

For the first time immunoreactive luteinizing hormone-releasing hormone (LH-RH) is demonstrated in both the brain and pituitary gland of a teleost (Xiphophorus maculatus) using an immunoperoxidase procedure. It is specifically localized in the perikarya and their axons of the ventral telencephalon and nucleus lateralis tuberis and within and between the gonadotrops and within some cells of the pars intermedia. These immunoreactions are extinguished when antiserum to LH-RH is preincubated with LH-RH antigen but not with neurohypophysial hormones.     

Concentrations of luteinizing hormone and oestradiol in plasma and response to injection of gonadotrophin-releasing hormone analogue at selected stages of anoestrus in domestic bitches.

Concentration of plasma luteinizing hormone (LH) and oestradiol concentrations and responses to a standard challenge with a gonadotrophin-releasing hormone (GnRH) analogue were measured at certain stages of anoestrus during consecutive cycles in five beagle bitches. Blood samples were collected every 20 min for 6h followed immediately by injection of GnRH analogue (0.16 micrograms i.v.) and collection of further samples after 10, 20, 40 and 60 min. Five, 10, 17 and three such sampling sequences were obtained during the luteal phase, transition to anoestrus, anoestrus and pro-oestrus respectively (i.e. 154-71, 114-44, 85-11 and 7-1 days before the preovulatory LH peak, respectively). Pulsatile LH secretion occurred spontaneously at all stages of the luteal phase and anoestrus and there was no effect of cycle stage on mean LH concentration or variability. In contrast, oestradiol could not be detected in most samples from early and mid-anoestrus until approximately one month before the preovulatory LH peak, after which average oestradiol concentration and between sample variability appeared to increase. Mean (+/- SEM) oestradiol concentration for all samples collected from 100-75, 74-50, 49-25, 24-10 and 9-1 days before LH peak was 1.4 +/- 0.1, 1.3 +/- 0.1, 2.4 +/- 0.3, 11.0 +/- 1.4 and 36.0 +/- 3.2 pg ml-1, respectively. Plasma LH concentration increased in all bitches after GnRH analogue injection (2.7 +/- 0.7 ng ml-1 at t = 0, 12.5 +/- 1.0 ng ml-1 at t = 10 min, mean +/- SEM, n = 35) regardless of cycle stage.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dissociation of cyclic AMP accumulation from that of luteinizing hormone (LH) release in response to gonadotropin releasing hormone (GnRH) and cholera enterotoxin.

Anterior hemipituitaries from female rats were incubated $\text{in}\text{vitro}$ in Krebs Ringer bicarbonate buffer, pH 7.2 containing 2 mg/ml of glucose in the absence and in the presence of GnRH or cholera enterotoxin. Following this incubation, the pituitaries were separated from the medium and cAMP and LH were assayed in the tissue and the medium, respectively. Incubations with GnRH in the range of 25 ng/ml to 400 ng/ml resulted in increase in LH release into the medium. Cholera enterotoxin at a concentration of 1 μg/ml, by contrast, caused no release of LH into the medium, but caused a 5-fold increase in cAMP level and this effect was concentration dependent. Cholera enterotoxin did not interfere with the GnRH-mediated LH release. It is concluded from these experiments that the ability of GnRH to increase cAMP level may be independent of its ability to release LH.     

Restoration of responsiveness to gonadotropin releasing hormone (GnRH) in calcium-depleted rat pituitary cells.

GnRH-stimulated, but not basal, luteinizing hormone (LH) release from cultured pituitary cells requires extra-cellular calcium. The present studies were designed to show whether cells which had lost responsiveness to GnRH in the absence of extracellular calcium (“Ca²⁺-depleted cells”) could regain responsiveness by readdition of calcium to the media. The addition of calcium-containing medium to cells which were preincubated (75 min) in calcium-free medium resulted in elevated basal LH release. Addition of GnRH to the media in the presence of calcium did not cause additional stimulation of LH release above the elevated basal level. Incubation of Ca²⁺-depleted cells in calcium-containing media for 2 h before measuring responsiveness depressed the basal level to near that seen in control cells and GnRH was able to stimulate LH release, but not to as high a level as in control cells (which were preincubated in 1 mM Ca²⁺-containing media). After incubation of calcium depleted cells in calcium-containing media for 3 h or 5 h, the basal and stimulated levels of LH response were statistically indistinguishable from those seen in control cells.     

Homologous desensitization of gonadotropin-releasing hormone (GnRH) receptors in the goldfish pituitary: effects of native GnRH peptides and a synthetic GnRH antagonist.

Gonadotropin-releasing hormone (GnRH) stimulates release of gonadotropin hormone (GTH) through interaction with high affinity receptors in the goldfish pituitary. In the present study, we investigated desensitization of two native GnRH peptides, [Trp7, Leu8]-GnRH (sGnRH) and [His5, Trp7, Tyr8]-GnRH (cGnRH-II), using superfused fragments of goldfish pituitary in vitro. Pulsatile treatment with either sGnRH or cGnRH-II (2-min pulses given every 60 min) resulted in dose-dependent secretion of GTH from the goldfish pituitary; cGnRH-II had a greater GTH release potency and displayed a greater receptor binding affinity than sGnRH. Both sGnRH and cGnRH-II-induced GTH release were partially inhibited by concomitant treatment with either [D-Phe2, Pro3, D-Phe6]-GnRH or [D-pGlu1, D-Phe2, D-Trp3.6]-GnRH. These antagonists had greater receptor binding affinities than the native peptides, with no stimulatory action on GTH release in the absence of the GnRH agonists. Continuous treatment with either sGnRH or cGnRH-II (10(-7) M), rapidly desensitized pituitary GTH release in a biphasic fashion; initially there was a rapid increase in GTH release of approximately 10-20-fold (phase 1), followed by a sharp decline in GTH release, reaching a stable concentration 2-3-fold above the basal level (phase 2). Further stimulation of the pituitaries with sGnRH or cGnRH-II (10(-7) M) (second treatment) after 60 min recovery resulted in a significantly lower sGnRH or cGnRH-II-induced GTH release compared to that observed during the initial treatment period.(ABSTRACT TRUNCATED AT 250 WORDS)     

Chloride channels mediate the response to gonadotropin-releasing hormone (GnRH) in Xenopus oocytes injected with rat anterior pituitary mRNA

Functional expression of receptors for GnRH was studied using Xenopus laevis oocytes injected with poly(A)+ mRNA extracted from rat anterior pituitary glands. Whole-cell currents were monitored using two-electrode voltage-clamp techniques. In oocytes which responded to both GnRH and TRH, the GnRH response showed a longer latency and time-to-peak than the TRH response. The response to GnRH or an agonist of GnRH receptors, buserelin (1 nM-1 microM) consisted of current fluctuations and occurred in a dose-dependent manner. This GnRH response was blocked by the Cl- channel blockers 9-AC (9-anthracene carboxylic acid; 1 mM), 4,4'-diisothiocyanastilbene-2,2'-disulfonic acid (0.1 mM), and diphenylamine-2-carboxylic acid (0.1 mM). The reversal potential for the GnRH-induced current fluctuations was -25 mV, comparable with the reported Cl- equilibrium potential in Xenopus oocytes, and its shift, when the external concentration of Cl- was changed, was reasonably described by the Nernst equation. These results indicate that the GnRH-induced response was dependent on the activity of Cl- channels. Ca2+ also plays a role, as the GnRH-induced response was reversibly suppressed by a calmodulin inhibitor, chlordiazepoxide (0.2 microM), and by a blocker of intracellular Ca2+ release, TMB-8 (8-(N.N-diethylamino) octyl-3,4,5-trimethoxybenzoate; 0.1-0.2 mM). It is concluded that GnRH (and TRH) receptors, expressed in Xenopus oocytes by injecting exogenous mRNA from rat anterior pituitary glands, operate via activation of Ca2+-dependent Cl- channels.     

Effect of adrenocorticotrophic hormone (ACTH1-24) on ovine pituitary gland responsiveness to exogenous pulsatile GnRH and oestradiol-induced LH release in vivo.

The present experiment was designed to determine if and how exogenous ACTH replicates the effects of stressors to delay the preovulatory LH surge in sheep. Twenty-four hours after oestrous synchronisation with prostaglandin in the breeding season, groups of 8-9 intact ewes were injected with 50 microg oestradiol benzoate (0 h) followed 8 h later by 3 injections of saline or GnRH (500 ng each, i.v.) at 2 h intervals (controls). Two further groups received an additional 'late' injection of ACTH (0.8 mg i.m.) 7.5 h after oestradiol, i.e., 0.5 h before the first saline or GnRH challenge. To examine if the duration of prior exposure to ACTH was important, another group of ewes was given ACTH 'early', i.e. 2.5 h before the first GnRH injection. The first GnRH injection produced a maximum LH response of 1.9+/-0.4 ng/ml which was significantly (p < 0.01) enhanced after the second and third GnRH challenge (7.1+/-1.5 ng/ml and 7.0+/-1.7 ng/ml, respectively; 'self-priming'). Late ACTH did not affect the LH response after the first GnRH challenge (1.9+/-0.4 vs. 1.8+/-0.3 ng/ml; p > 0.05) but decreased maximum LH concentrations after the second GnRH to 35% (7.1+/-1.5 vs. 4.6+/-1.1 ng/ml; p = 0.07) and to 40% after the third GnRH (7.0+/-1.7 vs. 4.0+/-0.8 ng/ml; p = 0.05). When ACTH was given early, 4.5 h before the second GnRH, there was no effect on this LH response suggesting that the effect decreases with time after ACTH administration. Concerning the oestradiol-induced LH surge, exogenous GnRH alone delayed the onset time (20.5+/-2.0 vs. 27.8+/-2.1 h; p > 0.05) and reduced the duration of the surge (8.5+/-0.9 vs. 6.7+/-0.6 h; p > 0.05). The onset of the LH surge was observed within 40 h after oestradiol on 29 out of 34 occasions in the saline +/- GnRH treated ewes compared to 11 out of 34 occasions (p < 0.05) when ACTH was also given, either late or early. In those ewes that did not have an LH surge by the end of sampling, plasma progesterone concentrations during the following oestrous cycle increased 2 days later suggesting a delay, not a complete blockade of the LH surge. In conclusion, we have revealed for the first time that ACTH reduces the GnRH self-priming effect in vivo and delays the LH surge, at least partially by direct effects at the pituitary gland.     

Studies on the effects of low doses of 5 alpha-dihydrotestosterone (DHT) on the basal levels of serum gonadotropins and the sensitivity of the pituitary to luteinizing hormone releasing hormone (LHRH) in adult male rats

Investigations were undertaken to study the effect of administering s.c. 10, 25, 50, 100, 500 and 1000 ng DHT/rat/day to normal adult male rats, for six weeks, on the basal levels of serum gonadotropin and the sensitivity of the pituitary to LHRH. The control group received olive oil. Animals were weighed and bled via cardiac puncture before the beginning of the treatment and weekly thereafter. After the last bleeding rats were injected intracardially 200 ng LHRH/rat and killed 15 min later. Blood, pituitary and testes were collected. Data were analyzed with respect to the control group and with respect to day zero of the treatment. DHT failed to produce a persistent effect on the serum gonadotropin. 10 and 500 ng DHT suppressed FSH levels significantly on days 21 and 7, respectively. 25, 50, 100 and 1000 ng DHT stimulated the release of FSH on day 42. 10 ng DHT reduced the levels of LH on day 14 of the treatment. 10, 25 and 50 ng DHT increased the sensitivity of the pituitary to release more LH in response to LHRH while 100, 500, 1000 ng DHT inhibited LHRH induced release of FSH. DHT at all doses tested failed to affect intrapituitary levels of LH and FSH. 10, 500 and 1000 ng DHT reduced the weights of the pituitaries as compared to the control group. The data demonstrate effects of DHT which are transient on the basal release of gonadotropins but are more persistent and differential on the sensitivity of the pituitary to LHRH.     

Use of a mammalian gonadotropin‐releasing hormone (GnRH) agonist to characterize pituitary GnRH receptors in white sturgeon (Acipenser transmontanus Richardson)

Aim of the present study was to characterize the pituitary GnRH receptor in white sturgeon, Acipenser transmontanus, using a superagonist analog of mammalian GnRH [D‐Ala⁶, des‐Gly¹⁰–Pro⁹]‐ethylamide and to investigate the possible effect of estradiol‐17β treatment on the concentration and affinity of the GnRH receptor in immature white sturgeon. The binding of ¹²⁵I‐GnRH‐A to sturgeon pituitary receptors was rapid and saturable at 4°C and 20°C. However, maximal binding at 20°C was almost two‐fold greater than the highest binding noted at 4°C. Specific binding of radioligand was directly related to the amount of tissue included in the assay system over the range of 5–20 mg fresh tissue equivalents per ml. The binding capacity of ¹²⁵I‐GnRH‐A with sturgeon pituitary tissue was much greater than radiolabeled GnRH. Administration of E₂ to immature sturgeon caused an almost two‐fold increase in GnRH‐A binding capacity (E₂ treated: Bmax = 2.87 fmoles 3 mg^?1 FTE; control: Bmax = 1.70 fmoles 3 mg^?1), and did not affect GnRH‐A binding affinity (E₂ treated: Ka = 0.13 × 10¹¹ m ^?1; control: Ka = 0.15 × 10¹¹ m ^?1). Overall, the study provides evidence that the GnRH analog is effective for characterizing the GnRH receptor in white sturgeon; however, more experimentation is necessary to determine whether E₂ administration to immature white sturgeon can increase the GnRH receptor capacity.     

Effects of medroxyprogesterone acetate (MAP) on ovarian antral follicle development, gonadotrophin secretion and response to ovulation induction with gonadotrophin-releasing hormone (GnRH) in seasonally anoestrous ewes

When ovulation is induced with gonadotrophin-releasing hormone (GnRH) in anoestrous ewes, a proportion of animals fail to form normal (full-lifespan) corpora lutea (CL). Progesterone treatment before GnRH prevents luteal inadequacy. It remains uncertain whether a similar effect, achieved with medroxyprogesterone acetate (MAP) from intravaginal sponges, is mediated by influences on growing ovarian follicles and/or secretion of gonadotrophic hormones, before and after GnRH treatment. Two experiments were performed, on 13 and 11 anoestrous Western white-faced ewes, respectively. Seven and six ewes, respectively, received MAP-containing sponges (60 mg) for 14 days; the remaining ewes served as untreated controls. To test the effect of timing of GnRH administration after pre-treatment with MAP-releasing sponges, GnRH injections (250 ng every 2h for 24h followed by a bolus injection of 125 microg of GnRH i.v.) were given either immediately (Experiment 1) or 24h after sponge removal in the treated ewes (Experiment 2). Ovarian follicular dynamics (follicles reaching >or=5mm in size) and development of luteal structures were monitored using transrectal ultrasonography. In Experiment 1, the mean ovulation rate (0.7+/-0.3 and 1.0+/-0.4) and proportion of ovulating ewes (57 and 67%, respectively) did not vary (P>0.05) between MAP-treated and control ewes. Normal (full-lifespan) CL were detected in 29% of treated and 67% of control ewes (P>0.05). In Experiment 2, the mean ovulation rate (2.3+/-0.2 and 1.2+/-0.6; P<0.05) and percentage of ewes with normal (full-lifespan) CL (100 and 40%, respectively; P<0.10) were greater in the treated compared to control ewes. In Experiment 1, the mean peak concentration of the GnRH-induced LH surge was lower (P<0.05) in MAP-treated than in control ewes. There were no significant differences between MAP-treated and control ewes in the characteristics of follicular waves, mean daily serum FSH concentrations, and secretory parameters of LH/FSH, based on intensive blood sampling conducted 1 day before sponging and 1 day before sponge removal. It is concluded that treatment with MAP has no effect on the tonic secretion of LH/FSH or follicular wave development in anoestrous ewes. However, the GnRH-stimulated LH discharge was attenuated in the ewes that received MAP-impregnated sponges for 14 days and were treated with GnRH immediately after sponge withdrawal. Ovulatory response and CL formation were increased when GnRH was administered 24 h after sponge removal.     

The response of the anterior pituitary and testes to synthetic luteinizing hormone-releasing hormone (LHRH) and the effect of castration on pituitary responsiveness in the maturing chicken fed aflatoxin

The responsiveness of the anterior pituitary to exogenous luteinizing hormone-releasing hormone (LHRH; 20 micrograms/kg body weight) and the subsequent stimulation of testosterone secretion by the testes was studied after administration of dietary aflatoxin (10 ppm) to 9-wk-old male chickens. In both control and aflatoxin-treated males, there were significant (p less than 0.05) increases in plasma luteinizing hormone (LH) concentrations following LHRH administration, which peaked at 5 min post injection and declined thereafter. Plasma testosterone levels increased soon after the LHRH injection in control males, secondary to elevated LH levels in the peripheral circulation, and continued to increase throughout the experimental period. In contrast, this LH-induced elevation in plasma testosterone was delayed in aflatoxin-treated males, with no substantial increase until 20 min post-LHRH injection. In a subsequent experiment, castration of aflatoxin-fed males resulted in an altered response to exogenous LHRH, as compared to their intact counterparts. Based on these data, it appeared that while the LH-secretory capacity of the anterior pituitary was not diminished in birds receiving aflatoxin, the testicular response to exogenous LHRH was altered during aflatoxicosis. Additionally, the effect of castration on plasma LH profiles after LHRH administration provides preliminary evidence for extra-testicular effects of dietary aflatoxin on reproduction in the avian male.     

Evidence for a role of protein kinase C in luteinizing hormone synthesis and secretion. Impaired responses to gonadotropin-releasing hormone in protein kinase C-depleted pituitary cells

The role of protein kinase C in luteinizing hormone (LH) release was analyzed in studies on the actions of phorbol esters and gonadotropin-releasing hormone (GnRH) in normal and protein kinase C (Ca2+/phospholipid-dependent enzyme)-depleted pituitary cell cultures. LH secretory responses of normal pituitary cells to GnRH were reduced but not abolished in Ca2+-deficient medium, consistent with the existence of extracellular Ca2+-dependent and -independent components of GnRH action. Both of these components could be elicited by treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA). The LH secretory responses to TPA and GnRH were additive only at low doses and converged to a common maximum at high concentrations of the agonists in the presence or absence of extracellular Ca2+. The release of stored LH by GnRH and TPA was accompanied by secretion of newly synthesized LH from 2 to 5 h during stimulation by either of the agonists. LH synthesis was increased in a progressive and dose-dependent manner by GnRH and TPA, and the ratio between newly synthesized and released hormone was near 1:2. TPA caused rapid and complete translocation of cytosolic protein kinase C to the particulate fraction of pituitary cells, followed by a progressive decrease in total enzyme content to approximately 10% after 6 h. Partial recovery of the cytosolic enzyme (to 20%) occurred after washing and reincubation for 15 h. Such kinase C-depleted cells showed prominent, dose-dependent reductions in the actions of GnRH and TPA on LH release and synthesis in both normal and Ca2+-deficient media. These observations support the hypothesis that protein kinase C participates in LH biosynthesis and secretion in pituitary gonadotrophs and is involved in the actions of GnRH upon these processes.     

An unexpected increase in pituitary sensitivity to gonadotrophin releasing hormone after treatment with porcine follicular fluid (inhibin) in immature hemicastrate rats

Porcine follicular fluid (PFF) contains a factor (inhibin or folliculostatin) which is reported to selectively inhibit the secretion of follicle-stimulating hormone (FSH) from the anterior pituitary gland. Chronic treatment of hemicastrate immature rats with PFF is able to partially inhibit the FSH-mediated hypertrophy of the remaining testis. However, the pituitaries from PFF-treated rats are paradoxically very sensitive to stimulation with gonadotrophin-releasing hormone (GnRH) and secrete significantly more FSH than control glands. Furthermore, this increased sensitivity results in a large increase in luteinizing hormone (LH) secretion. These observations suggest that under certain circumstances PFF is not selective for FSH and that it surprisingly stimulates rather than inhibits gonadotrophin secretion.     

Thyroidal radioiodine uptake and thyrotropic potency of the pituitary in a freshwater catfish,Mystus vittatus (Bloch), in response to L-thyroxin,antithyroid drugs,and heavy doses of 131I

Summary Experiments were conducted to ascertain the thyroidal ¹³¹I uptake and thyrotropic potency of the pituitary gland in a freshwater catfish, in response to L-thyroxine, antithyroid drugs and heavy doses of radioiodine. L-thyroxine treatments slightly lowered thyroidal radioiodine uptake, and there was at least a trend of lowered TSH content in the pituitaries of these animals. Administration of antithyroid drugs (propylthiouracil, thiourea, KSCN) caused a significant decrease in radioiodine uptake and a highly significant increase in TSH content of the pituitary. Heavy doses of I¹³¹ almost completely blocked thyroidal iodine uptake but they were as effective as antithyroid drugs in elevating TSH content of the pituitary.I am greatly indebted to Dr. G. E. Pickford, Yale University, U.S.A. for her helpful suggestions; to Dr. A. G. Sathyanesan, Banaras Hindu University, India, for encouragements; to Professor S. P. Ray-Chaudhuri, Banaras Hindu University, India, for providing laboratory facilities. I am also grateful to Baxtor Laboratories Inc., Morton Grove, Illinois, U.S.A. for the gift of Crystalline L-thyroxine which was made available through the courtesy of Professor Paul Starr and Dr. Thomas Garrett.