Synthetic LH-releasing Hormone Research Articles

The participation of the muscarinic receptors in the preoptic-anterior hypothalamic areas in the regulation of ovulation depends on the ovary.

BackgroundMuscarinic receptors (mAChRs) of the preoptic and anterior hypothalamus areas (POA-AHA) regulate ovulation in an asymmetric manner during the estrous cycle. The aims of the present study were to analyze the effects of a temporal blockade of mAChRs on either side of the POA-AHA performed in diestrus-2 rats on ovulation, the levels of estradiol, follicle stimulating hormone (FSH) and luteinizing hormone (LH) and the mechanisms involved in changes in ovulation.MethodsCyclic rats on diestrus-2 day were anesthetized and randomly assigned to the following groups: 1) microinjection of 1 μl of saline or atropine solution (62.5 ng) in the left or right POA-AHA; 2) removal (unilateral ovariectomty, ULO) of the left (L-ULO) or right (R-ULO) ovary, and 3) rats microinjected with atropine into the left or right POA-AHA plus L-ULO or R-ULO. The ovulation rate and the number of ova shed were measured during the predicted estrus, as well as the levels of estradiol, FSH and LH during the predicted proestrus and the effects of injecting synthetic LH-releasing hormone (LHRH) or estradiol benzoate (EB).ResultsAtropine in the left POA-AHA decreased both the ovulation rate and estradiol and LH levels on the afternoon of proestrus, also LHRH or EB injection restored ovulation. L- or R-ULO resulted in a lower ovulation rate and smaller number of ova shed, and only injection of LHRH restored ovulation. EB injection at diestrus-2 restored ovulation in animals with L-ULO only. The levels of estradiol, FSH and LH in rats with L-ULO were higher than in animals with unilateral laparotomy. In the group microinjected with atropine in the left POA-AHA, ovulation was similar to that in ULO rats. In contrast, atropine in the right POA-AHA of ULO rats blocked ovulation, an action that was restored by either LHRH or EB injection.ConclusionsThese results indicated that the removal of a single ovary at noon on diestrus-2 day perturbed the neuronal pathways regulating LH secretion, which was mediated by the muscarinic system connecting the right POA-AHA and the ovaries.

Unilaterally blocking the muscarinic receptors in the suprachiasmatic nucleus in proestrus rats prevents pre-ovulatory LH secretion and ovulation.

BackgroundThe suprachiasmatic nucleus (SCN) and the cholinergic system of various regions of the hypothalamus participate in the regulation of gonadotropin-releasing hormone (GnRH) and gonadotropin secretion, which are necessary for the occurrence of ovulation. In the present study, our goal was to analyse the effects of unilaterally blocking the muscarinic receptors in the SCN on ovulation and steroid secretion.MethodsCyclic rats were randomly allotted to one of the experimental groups. Groups of 8–14 rats were anaesthetized and microinjected with 0.3 μl of saline or a solution of atropine (62.5 ng in 0.3 μl of saline) into the left or right SCN at 09.00 or 19.00 h during diestrus-1 or on the proestrus day. The rats were euthanized on the predicted day of oestrus, and evaluated ovulation and levels of progesterone and oestradiol. Other groups of 10 rats were microinjected with atropine into the left or right SCNs at 09.00 h on the proestrus day, were euthanized eight h later, and luteinizing hormone (LH) was measured.ResultsAt 09.00 or 19.00 h during diestrus-1, atropine microinjections into the SCNs on either side did not modify ovulation. The atropine microinjections performed at 09.00 h of proestrus into either side of the SCN blocked ovulation (right SCN: 1/9 ovulated vs. 9/10 in the saline group; left SCN: 8/14 ovulated vs. 10/10 in the saline group). The LH levels at 17.00 h in the rats that were microinjected with atropine at 09.00 h of proestrus were lower than those of the controls. In the non-ovulating atropine-treated rats, the injection of synthetic LH-releasing hormone (LHRH) restored ovulation. Atropine treatment at 19.00 h of proestrus on either side of the SCN did not modify ovulation, while the progesterone and oestradiol levels were lower.ConclusionBased on the present results, we suggest that the cholinergic neural information arriving on either side of the SCN is necessary for the pre-ovulatory secretion of LH to induce ovulation. Additionally, the regulation of progesterone and oestradiol secretion by the cholinergic innervation of the SCN varies with the time of day, the day of the cycle, and the affected SCN.

On the effect of synthetic LH-releasing hormone on the blood levels of LH, FSH, HGH, TSH, ACTH, insulin and blood sugar in man.

On the effect of synthetic LH-releasing hormone on the blood levels of LH, FSH, HGH, TSH, ACTH, insulin and blood sugar in man.

Feedback of Follicle-Stimulating Hormone to Inhibit Luteinizing Hormone and Stimulate Follicle-Stimulating Hormone Release in Ovariectomized Rats

Injection of ovine follicle-stimulating hormone (o-FSH) into the third cerebral ventricle significantly suppressed plasma luteinizing hormone (LH) release in conscious, unrestrained ovariectomized rats. Intraventricular injection of o-FSH (0.5 microgram) significantly lowered the plasma levels of LH by 70 min and decreased pulse frequency, whereas the pulsatile release of FSH was unchanged during the 180-min duration of the experiment. In a 12-hour experiment, the suppression of LH release reached the maximum within 3 h (p less than 0.001), followed by a return of plasma LH level to initial values 6-8 h after intraventricular injection of o-FSH at doses of 0.5, 4 and 8 micrograms. Plasma levels of FSH were not significantly changed by the low dose of o-FSH (0.5 microgram), but there was a delayed elevation of plasma FSH during the 8-12 h after intraventricular injection of o-FSH at higher doses (4 and 8 micrograms). On the other hand, plasma prolactin was unchanged after intraventricular injection of o-FSH. Since the pituitary responsiveness to synthetic LH-releasing hormone (LHRH) was unimpaired at the end of the sampling and incubation with o-FSH suppressed the release of LHRH from median eminence terminals, these data indicate that FSH acts intrahypothalamically to suppress LHRH release. The late elevation of plasma FSH may be the result of enhanced release of FSH-releasing factor or of a delayed, direct effect of the hormone on the gonadotropes to increase release of FSH.(ABSTRACT TRUNCATED AT 250 WORDS)

A comparative in vitro study on LHRH responsiveness of LH cells of the pars tuberalis and pars distalis.

The aim of the present study was to test whether the luteinizing-hormone (LH) cells in the pars tuberalis (PT) of the rat and mouse respond to LH-releasing hormone (LHRH) as do those of the pars distalis. A part of the basal hypothalamus containing the pituitary stalk, median eminence and the pars tuberalis (H-PT), was dissected out and incubated in vitro. The LH-secreting capacity of the PT was investigated after removal of the "pituitary body" (i.e., partes distalis, intermedia and nervosa). First, some rat and mouse H-PT tissues were treated with synthetic LHRH (100 ng/ml), while others were incubated without LHRH. After 24 h of incubation, variable amounts of LH release were detected in the medium. This LH discharge, however, was not LHRH-dependent but proportional to the number of PT LH cells that were immunohistochemically detected in each incubated tissue. Since there was marked individual variation in the number of LH cells in the PT, the LH levels in the incubation medium were next compared before and after LHRH treatment using the same H-PT of the rat. An effect of LHRH could not clearly be shown in this experiment. Finally, the cytological response of the PT to LHRH was investigated by incubating both the H-PT and pituitary body connected to the intact pituitary stalk. Immunohistochemical examination of LHRH-treated tissues after 24 h revealed that, in females of both rats and mice, hormone depletion occurred in LH cells of the pars distalis but not in those of the PT.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of oestradiol, phenobarbitone and luteinizing hormone releasing hormone upon the isoelectric profile of pituitary follicle-stimulating hormone in ovariectomized hamsters.

Anterior pituitary glands were removed from ovariectomized hamsters after specific endocrine treatments. The presence and relative proportions of the multiple species of FSH present within them were assessed by radioimmunoassay after separation by chromatofocusing. This technique is superior to polyacrylamide gel-isoelectric focusing, as it can accommodate a greater sample volume and has increased resolution. Endocrine conditions which decreased hypothalamic LH releasing hormone (LHRH) release or the sensitivity of the pituitary gland to that neurohormone (phenobarbitone treatment or short-term oestradiol exposure) caused an increase in the relative proportions of the more acidic forms (isoelectric points (pI) 5.1-3.8) of pituitary FSH and a concomitant reduction in the more basic (pI values 6.0-5.3) forms of FSH. During times of increased pituitary LHRH exposure (immediately before the oestradiol-induced gonadotrophin surge or after injection of synthetic LHRH) an increase was observed in the relative proportion of the more basic forms of pituitary FSH. Treatment of ovariectomized hamsters with an inhibin-containing preparation reduced serum FSH concentrations as well as the relative proportion of the more basic forms of pituitary FSH. We have previously shown that the more studies suggest that the existing hormonal milieu, in particular LHRH and oestradiol, influences the types of FSH produced and (presumably) secreted. Thus, through hormonal interactions, the pituitary gland regulates not only the absolute amount but also the potency of the FSH signal to the ovaries.

Purification of a bioactive FSH-releasing factor (FSHRF)

Before the advent of radioimmunoassay (RIA), FSH-releasing factor (FSHRF) appeared to be separable from LH-releasing hormone (LHRH) by chromatography followed by bioassay for FSH. In this study, we re-examined hypothalamic extracts for the existence of an FSHRF distinct from LHRH, utilizing the Steelman-Pohley bioassay as well as RIA for identification of PSH. Acid extracts of rat hypothalamic fragments were chromatographed on Sephadex G-25. LH- and FSH-releasing activities of each fraction were assessed by bio- and immunoassay of FSH and immunoassay of LH released after incubation with hemipituitaries from adult male rats. The immunoreactive LHRH(IR-LHRH) concentration of each fraction was also measured by RIA. In order to evaluate the FSH-releasing activity of LHRH, three doses of synthetic LHRH were tested and FSH-releasing activity determined by bio- and immunoassay. By RIA, the FSH-releasing activity of each column fraction could be accounted for by IR-LHRH contamination. However, greater FSH-releasing activity than could be predicted by IR-LRH contamination was detected by Steelman-Pohley assay in fractions eluted prior to the LHRH peak in 2 separate fractionations. These fractions from the second fractionation were pooled and eluted from a CMC column with ammonium acetate buffers. Again greater FSH-releasing activity than could be accounted for by IR-LHRH was detected prior to the IR-LHRH peak by Steelman-Pohley assay. These results agree with early work from our laboratory and suggest the presence of a bioactive FSHRF in hypothalamic extracts.

Feedback effect of oestrogen on luteinizing hormone secretion by the rat pituitary gland.

Ovariectomized rats with neural deafferentation at the level of the posterior border of the anterior hypothalamic area (AC rats) were used to re-evaluate the direct feedback effect of oestrogen on the regulation of LH secretion by the pituitary gland. Synthetic LH releasing hormone (LH-RH; 300 ng/kg), injected at 30 min intervals into AC rats with undetectable basal LH, induced pulsatile increase of serum LH concentrations. Oestradiol-7Beta (5 micrograms), administered i.v. just before the first LH-RH injection, significantly decreased the LH response to a second injection of LH-RH given 30 min later and to subsequent injections. Maximal inhibition was 58%. Oestradiol 17 beta (5 micrograms) given i.v. to control ovariectomized rats decreased serum LH concentrations 40 min after administration; the maximum reduction being 52%. An s.c. injection of oestradiol benzoate (5 micrograms) increased pituitary responsiveness to LH-RH by the next day in AC rats but decreased serum LH levels in control ovariectomized rats. These results indicate that acute inhibitory and chronic facilitatory effects of oestrogen on LH secretion are exerted at the pituitary gland, without a change in LH-RH secretion. The prolonged inhibitory effect of oestrogen is at the level of the hypothalamus and causes a reduction in LH-RH secretion.

Decapeptide luteinizing hormone releasing hormone in ovine pineal gland.

Ovine pineal gland extracts were examined throughout the year for content and molecular form of immunoreactive (IMR) LH releasing hormone (LH-RH). The content of IMR LH-RH in pineal glands collected in spring and summer was 160-2230 pg/gland, while the content in pineal glands collected in autumn and winter was lower (31-39 pg/gland). Pineal gland IMR LH-RH, purified by affinity and Sephadex G-25 chromatography, yielded displacement curves parallel to those of hypothalamic IMR LH-RH and synthetic LH-RH in radioimmunoassays employing four antisera which require different regions of the decapeptide for effective binding, suggesting considerable similarities in the structure of the molecule. The majority of pineal gland IMR LH-RH behaved identically to hypothalamic IMR LH-RH and synthetic LH-RH on gel filtration, cation exchange chromatography, high-pressure liquid chromatography and cellulose thin-layer chromatography. However, a small amount of a less positively charged LH-RH species was also present in all pineal gland extracts. Our findings indicate that hypothalamic decapeptide LH-RH occurs in the ovine pineal gland.

Response of luteinizing hormone from columns of dispersed rat pituitary cells to a highly potent analogue of luteinizing hormone releasing hormone.

The response of LH from a perfused column of dispersed rat anterior pituitary cells to LH releasing hormone (LH-RH) and the analogue, D-Ser(But)6-desGly10-Proethylamide9-LH-RH (Hoe 766), was investigated. Dose-response curves showed non-parallelism between LH-RH and the analogue. but it was evident that the analogue was considerably more potent. After a single pulse of LH-RH, LH output returned to basal values in 8 min; this was prolonged to 20 min in the case of the analogue. During this 20 min the cells were refractory to pulses of LH-RH but pulses of the analogue maintained output of LH. During constant-dose perfusion with either synthetic LH-RH or the analogue, output of LH rapidly reached a peak and then gradually fell over several hours to approach baseline values. However, a pulse of 50 mmol potassium chloride/l was still able to release LH at this time. The data are consistent with the view that this analogue of LH-RH is highly potent and is strongly bound by the LH-RH receptor. Furthermore, since it desensitizes the LH-RH receptor, it appears that continued turnover of either LH-RH or the analogue at the receptor is necessary for output of LH to be maintained.

Effects of oestradiol, hypothalamic extracts and luteinizing hormone releasing hormone on rat anterior pituitary gland gonadotrophin release in vitro before and after the preovulatory luteinizing hormone surge at pro-oestrus.

Changes at the anterior pituitary and/or hypothalamic levels which result in selective FSH release during late pro-oestrus in the cyclic rat were investigated. The possible involvement of decreasing serum concentrations of oestrogen during pro-oestrus in such changes was studied. Rats were decapitated at 12.00 h on pro-oestrus, before the onset of the LH surge and first phase of FSH release, or at 24.00 h on pro-oestrus, shortly after the onset of the second or selective phase of FSH release. Other rats were given oestrogen (OE2) at 14.00 h and killed at 24.00 h pro-oestrus. Paired hemi-anterior pituitary glands were incubated with vehicle or OE2 with or without synthetic LH-releasing hormone (LH-RH) or hypothalamic acid extracts prepared from rats killed at 12.00 or 24.00 h on pro-oestrus. At 24.00 h pro-oestrus, serum FSH concentration was high while serum LH concentration was low regardless of whether rats were given OE2. Glands collected and incubated at 24.00 h released more FSH and less LH than did glands collected and incubated at 12.00 h pro-oestrus. Administration of OE2 in vivo and/or in vitro did not affect these responses. The increments in LH and FSH release attributed to LH-RH or hypothalamic extracts in the glands incubated at 24.00 h were not different from those of the glands incubated at 12.00 h. Also, the hypothalamic extracts prepared from rats killed at 24.00 h were no more effective than the extracts prepared from rats killed at 12.00 h in releasing LH or FSH from glands incubated at 12.00 or 24.00 h pro-oestrus. Administration of OE2 in vivo caused a small suppression of LH-RH-induced FSH release. We suggest that a change occurs at the level of the anterior pituitary gland during the period of the LH surge and first phase of FSH release to increase basal FSH secretion selectively and cause, at least in part, the second phase of increased serum FSH. This change is not mediated by a decrease in serum oestrogen concentration. We failed to observe any evidence that LH-RH causes preferential FSH release during late pro-oestrus or that a hypothalamic peptide with a preferential FSh releasing ability is involved in FSH release at this time.

EFFECTS OF AN ANTI-OESTROGEN, TAMOXIFEN (ICI 46,474), ON LUTEINIZING HORMONE RELEASE AND OVULATION IN THE HEN

The role of oestradiol in the regulation of LH release in the hen was studied by use of the anti-oestrogen, tamoxifen (ICI 46,474). Intramuscular injection of laying hens with 2 or 4 mg tamoxifen on 2 successive days delayed or prevented the occurrence of the preovulatory release of LH and ovulation expected on day 3. Ovulation could be restored by i.v. injection of 20 micrograms LH releasing hormone (LH-RH). Tamoxifen at a dose of 1 mg affected neither the timing of the preovulatory release of LH nor ovulation. Treatment with 2 or 4 mg tamoxifen on 2 successive days reduced the effectiveness of an i.m. injection of progesterone to stimulate a release of LH. Injection of 1, 2 or 4 mg tamoxifen on 2 successive days significantly raised basal levels of LH in the blood at 24 h after the last injection. This was associated with an increase in the capacity of the pituitary gland to respond to an injection of synthetic LH-RH by a release of LH. These studies suggest that oestradiol has at least two roles in the regulation of LH release in the hen. First, it maintains a low basal level of LH-RH. Secondly, oestradiol has a facilitative role in the mechanism by which progesterone stimulates the preovulatory release of LH.

Chromatographic and biologic analysis of ME and OVLT LHRH

The luteinizing hormone (LH)-releasing activities of pooled rat organum vasculosum lamina terminalis (OVLT) and median eminence (ME) tissues were evaluated for chromatographic and biologic similarity and compared to those of synthetic decapeptide LH-releasing hormone (LHRH). The LHRH detected in these extracts appeared similar chromatographically (Sephadex G-25) to synthetic LHRH. These extracts, as well as synthetic LHRH, were also capable of stimulating dose dependent gonadotropin release from cultured rat gonadotrophs. These findings suggest a physiological role of the LHRH present in the rat OVLT in the control of gonadotropin secretion.

USE OF A PULSED INFUSION OF LUTEINIZING HORMONE RELEASING HORMONE TO MIMIC SEASONALLY INDUCED ENDOCRINE CHANGES IN THE RAM

Adult Soay rams were housed indoors under natural lighting during the spring non-mating season when gonadotrophin secretion was low. Four animals received small doses (100 ng or 500 ng) of synthetic LH releasing hormone (LH-RH) infused into the jugular vein by a mechanical device for 60 s every 2 h for 33-57 days: two other rams acted as controls. The prolonged treatment with LH-RH resulted in growth of the testes and the development of the sexual skin flush; these effects were lost when treatment stopped. The plasma concentrations of LH, FSH and testosterone were low at the beginning; each short infusion of LH-RH resulted in a transitory increase in the level of LH and testosterone while the concentration of FSH was only marginally affected. After prolonged treatment with 500 ng pulses of LH-RH the plasma concentrations of all three hormones were permanently raised. The response to the individual injections of LH-RH was also modified, the peak in LH being reduced in amplitude but more prolonged while the FSH and testosterone responses were both enhanced. When the pulsed infusion was stopped the concentration of LH and testosterone declined rapidly while the decline in FSH levels took many days. These endocrine changes induced by the pulsed infusion are comparable to those that occur naturally in the ram during testicular redevelopment before the mating season.

POSSIBLE PRIMING EFFECT OF LUTEINIZING HORMONE RELEASING HORMONE ON THE ANTERIOR PITUITARY GLAND IN THE JAPANESE QUAIL AND THE STIMULATION OF SECRETION OF FOLLICLE-STIMULATING HORMONE

After the i.m. injection of 10 micrograms synthetic LH releasing hormone (LH-RH) into Japanese quail the levels of LH and FSH in plasma rose significantly within 2 min. The increased level of LH declined rapidly but that of FSH was maintained for the duration of the experiment. To determine whether the anterior pituitary gland is primed by LH-RH a double injection schedule was adopted. It would appear that, while endogenous LH-RH may prime the avian pituitary gland slightly, synthetic LH-RH is ineffective.

Synchronization of estrus and ovulation with in-tramuscular injection of prostaglandin F<SUB>2α</SUB> followed by additional synthetic LH-releasing hormone in the cow

Synchronization of estrus and ovulation with in-tramuscular injection of prostaglandin F<SUB>2α</SUB> followed by additional synthetic LH-releasing hormone in the cow

PHOTOPERIODIC CONTROL OF REPRODUCTION IN JAPANESE QUAIL: CHANGES IN GONADOTROPHIN SECRETION ON THE FIRST DAY OF INDUCTION AND THEIR PHARMACOLOGICAL BLOCKADE

SUMMARY Photoperiodic processes often seem rather slow because the induced developmental changes, such as gonadal growth in a seasonally breeding bird, may take many weeks to reach completion. This is rather deceptive, however, as initial changes occur rapidly. Following the transfer of sexually immature Japanese quail to a photoperiod of 20 h light:4 h darkness (20L:4D), plasma levels of both LH and FSH remained low on the first day of treatment until 18 h after the onset of light when they both rose significantly. Over the next few hours the levels of both hormones rose three- to fourfold. In a more detailed experiment in which blood samples were collected every 2 h, the mean LH concentration showed no increase before hour 20 but rose significantly from 0·92± 0·09 (s.e.m.) to 1·67± 0·19 ng/ml (n = 6) between hours 20 and 22. By hour 26 the mean LH level had reached 2·68 ± 0·25 ng/ml. To determine the light-sensitive period on the first day of photostimulation, immature quail were transferred from short days (8L: 16D) to one of the following photoperiods: 12L: 12D, 13·3L: 10·7D, 14·7L: 9·3D, 16L: 8D, 20L: 4D or to continuous light. Blood samples were collected at hours 12, 19 and 25 after the onset of light. The concentration of LH did not change in the groups exposed to 12L:12D or to 13·3L:10·7D. In all other groups, however, it increased significantly between hours 19 and 25 regardless of whether the quail were in darkness or light, or whether a light/dark transition occurred. The magnitude of the rise was similar in the four stimulatory photoperiods. These results indicate that light before the twelfth hour is not photoperiodically effective but that further exposure to 3 h or more light from hour 12 causes induction after a lag of some hours, and an increase in LH at the end of the first day. When the LH rise was observed over 2 consecutive long days the response seemed to occur earlier on the second than on the first day. To see whether the delay in the rise of LH secretion until hour 20 was due to a change in the sensitivity of the pituitary gland to LH releasing hormone (LH-RH), birds were tested in three experiments. 'Short-day' quail were injected i.m. with two equal doses of synthetic LH-RH, the second dose being given 30, 60 or 90 min after the first. The results indicated that the first dose of LH-RH did not enhance the amount of LH released by the second dose. In fact, the response to the second dose was significantly less. Similarly, an injection of LH-RH at hour 12 did not advance the LH response on the first long day. Finally, the sensitivity of the pituitary gland to exogenous LH-RH was determined at various times on the first long day. No augmented responsiveness was observed at hours 22 and 24. It would appear, therefore, that the lag may not be in the pituitary gland but may exist in neural or neuroendocrine events which occur in the brain of the quail between hours 12 and 16 and which lead to enhanced gonadotrophin secretion beginning at about hour 20 on the first long day.

ROLE OF GONADOTROPHIN RELEASING HORMONES IN THE REPRODUCTIVE BEHAVIOUR OF FEMALE RING DOVES (STREPTOPELIA RISORIA)

This work was carried out to determine whether gonadotrophin releasing hormone(s) (GnRH) plays a role in the courtship behaviour of female ring doves. In particular, it tests the hypothesis that a high dose of oestrogen suppresses the synergistic action of GnRH with oestrogen which is required to elicit courtship behaviour. The hypothesis was formulated to provide an explanation for a finding in a previous study that ovariectomized ring doves treated with a high dose of oestrogen, paradoxically, failed to show courtship behaviour. In the present study, treatment with synthetic LH releasing hormone (RH) enabled such birds to show typical female behaviour, thus supporting the hypothesis. This LH-RH effect was not apparently mediated by LH or progesterone since treatment with LH or progesterone failed to induce courtship behaviour. In addition, LH-RH can synergise with sub-threshold doses of oestrogen to induce both nest-soliciting and squatting behaviour. This portion of the LH-RH effect complements similar results reported for the rat. Finally, the results of thyrotrophin releasing hormone point to the specificity of LH-RH and the results of an anti-ovulation LH-RH analogue agree with the LH-RH effect.

AN HOMOLOGOUS RADIOIMMUNOASSAY FOR CHICKEN FOLLICLE-STIMULATING HORMONE: OBSERVATIONS ON THE OVULATORY CYCLE

A highly purified FSH preparation has been used to develop a specific homologous radioimmunoassay for chicken FSH which is sufficiently sensitive and precise to measure the hormone in small sample (10-100 microliter) of plasma. The assay was used to measure plasma FSH in the chicken and turkey. The FSH concentration was higher in sexually mature chickens than in juvenile birds and further elevated after castration or ovariectomy. In turkeys, it was lower in birds held on a short daily photoperiod than in birds held on a long daily photoperiod. FSH rose in sexually quiescent female turkeys after injection of synthetic LH-releasing hormone and was increased in laying hens after injection of progesterone. No major changes were observed in FSH concentration during the chicken ovulatory cycle, although there was a small increase 15 and 14 h before ovulation.

Increased Responsiveness to LH-Releasing Hormone (LHRH) in Rats with Median Eminence Lesions

SummaryResponsiveness to synthetic LHRH, as measured by increments in plasma LH following its sc injection, was evaluated in castrated rats with median eminence lesions and compared to that in sham-operated controls and controls with intact brains. Median eminence lesions in castrates were followed by a decline in plasma LH to approximately 30% of control values at 1, 7, and 14 days postlesions. This was associated with an increase in responsiveness to LHRH at 1 day, followed by a return to normal responsiveness at 7 and 14 days postlesions. Even though plasma LH was lowered in the animals with lesions, pituitary LH was little changed, which indicates that these lesions, although effective to inhibit LH release, were probably incomplete.It is concluded that LH release is inhibited by lesions in the median eminence in the face of normal or even increased responsiveness to LHRH. The cause of the increased responsiveness to LHRH which appeared at 1 day after lesions remains to be elucidated.