Ovulatory Surge Of Luteinizing Hormone Research Articles

Reproductive endocrine patterns in captive female and male red wolves (Canis rufus) assessed by fecal and serum hormone analysis

AbstractReproductive steroid profiles in female (n=13) and male (n=5) red wolves (Canis rufus) were characterized in fecal samples collected during the breeding season (December—May) and over a 1 year period, respectively. Blood samples from females (n=12) also were collected during the periovulatory period for luteinizing hormone (LH) and steroid analysis. High performance liquid chromatography (HPLC) of fecal extracts determined that estradiol and estrone constituted the major and minor forms, respectively, of fecal estrogen metabolites. Although native progesterone was present, pregnane metabolites predominated as the major forms of fecal progestins. HPLC analysis of fecal extracts from males revealed no native testosterone, but rather the predominance of more polar androgen metabolites. Based on hormone profiles and/or pup production, females were classified as pregnant (n=3), ovulatory‐nonpregnant (n=9), or acyclic (n=3). Longitudinal monitoring of females indicated no pregnancy‐specific differences in concentrations of either fecal progestagen or estrogen metabolites compared to ovulatory‐nonpregnant individuals; however, baseline progestagen concentrations were consistently elevated in acyclic females. There was good correspondence between serum and fecal steroid concentration during the periovulatory period. A rise in serum estrogens preceded the ovulatory LH surge which was then followed by a significant progesterone rise during the luteal phase. In males, changes in fecal androgen metabolite concentrations coincided with photoperiod fluctuations, increasing in late autumn and reaching peak concentrations during mid‐ to late winter just before the start of the breeding season. Collectively, these results serve as a database of ovarian and testicular endocrine events in this species, which can be utilized in population management and application of assisted reproductive technologies. Zoo Biol 21:321–335, 2002. © 2002 Wiley‐Liss, Inc.

Reproductive endocrine monitoring of elephants: An essential tool for assisting captive management

Considerable information now is available about the basic reproductive biology of elephants, especially females. However, as important as this knowledge is, it no longer is enough to simply compile it into a database. The potential exists for using endocrine monitoring techniques to solve real problems. This review summarizes our current knowledge of elephant endocrinology and offers suggestions on how to use the technology to maximize reproductive potential. The estrous cycle can be monitored through the analysis of serum progestogens, primarily 5α-reduced compounds, and consists of an 8- to 12-week luteal phase and a 4- to 6-week inter-luteal period. Proof of ovarian cyclicity currently is mandatory before Species Survival Plan breeding recommendations are approved. However, because many adult females are not cycling normally, the reproductive monitoring of all cows throughout their life span is now encouraged. Complete endocrine evaluations in conjunction with ultrasound examinations and behavioral assessments are needed to identify causes of reproductive failure and develop mitigating treatments. Progestogen analyses also are effective for monitoring pregnancy, but only if longitudinal samples are collected. Alternatively, pregnancy can be diagnosed in occasional samples using serum prolactin or possibly relaxin measurements after 20 weeks of gestation. Parturition can be predicted on the basis of the rapid decrease in progestogens that occurs about 2–5 days before birth. An updated model of ovarian dynamics during the estrous cycle suggests that two waves of follicular development occur 3 weeks apart during the non-luteal phase, possibly under the control of follicle-stimulating hormone. Each follicular wave culminates in a luteinizing hormone (LH) surge, with the second surge inducing ovulation and corpus luteum formation. The functional significance of the first, anovulatory LH surge is under investigation, but from a practical perspective it can be used to schedule breeding (by artificial insemination or natural mating) to coincide with the ovulatory LH surge. Less is known about the reproductive biology of bulls, aside from the fact that musth is associated with dramatic changes in androgen secretion. Studies are needed to determine whether poor libido and inadequate semen quality observed in some mature elephants are due to testicular steroidogenic dysfunction. When blood samples cannot be collected for routine hormone analysis, gonadal activity can be monitored non-invasively through the measurement of excreted steroid metabolites (males: androgens; females: estrogens, progestogens) in urine and feces. Lastly, suggestions for future research priorities are provided. Zoo Biol 19:347–367, 2000. © 2000 Wiley-Liss, Inc.

Ultrasonography of the estrous cycle in female African elephants (Loxodonta africana)

The endocrinology of the elephant estrous cycle has been well characterized, but little emphasis has been placed on evaluating corresponding changes in the reproductive tract. Ultrasound was used to document changes in reproductive tract morphology throughout the estrous cycle in four cycling female African elephants. During a 7-month period, frequent ultrasound examinations (n = 190) during the luteal and non-luteal phase were compared with serum progesterone and luteinizing hormone (LH) concentrations during a 7-month period. Ultrasonographic images documented vaginal and cervical edema and changes in mucus consistency during the non-luteal phase. The cross-sectional diameter of the endometrium showed a dramatic increase during the non-luteal phase and followed cyclic changes. A different pattern of follicular development on the ovary was associated with the two LH surges. Follicle growth associated with the first, anovulatory LH surge was characterized by the formation of multiple small follicles, in contrast to the maturation of a single large follicle at the second, ovulatory LH (ovLH) surge. Ovulation and the subsequent formation of a corpus luteum (CL) were observed only after the ovLH surge. Ultrasound data in combination with endocrine assessments suggest that the African elephant is non-ovulatory, although multiple non-ovulatory luteal structures developed during the late nonluteal phase of each cycle. Both ovulatory CL and non-ovulatory luteal structures were present only through one cycle and regressed at the end of the luteal phase in conjunction with the drop in serum progesterone. We conclude that

The effect of blockade of κ-opioid receptors in the medial preoptic area on the luteinizing hormone surge in the proestrous rat

The present study examined whether blockade of κ-opioid receptors in the medial preoptic area (MPOA) prior to the critical period on the afternoon of proestrus could prematurely evoke an ovulatory luteinizing hormone (LH) surge, and if so, whether norepinephrine (NE) is involved in mediating this response. In the first experiment, push–pull perfusion of the MPOA with nor-binaltorphimine (nor-BNI), a specific κ-opioid receptor antagonist, was done in rats between 10.30 and 13.50 h on proestrus. To determine whether any resulting ovulation was due to a nor-BNI-induced increase in LH release, rats were injected with pentobarbital at 13.55 h to block the afternoon LH surge. In 7 of 10 rats, nor-BNI in the MPOA produced a large increase in LH release beginning between 12.30 and 13.30 h, and 5 of 7 ovulated. During MPOA perfusion with cerebrospinal fluid in our normal colony between 14.00 and 17.00 h, surges of LH release began in the majority of rats between 15.30 and 16.30 h. Thus blockade of MPOA κ-opioid receptors advanced the LH surge by 3 h. The next experiment examined the effect of NE synthesis inhibition with bis(4-methyl-1-homopiperazinylthiocarbonyl) disulfide (FLA-63), or α-adrenergic receptor blockade with phenoxybenzamine (PBZ), on the nor-BNI-induced LH response. In 5 of 6 vehicle-treated rats, blockade of MPOA κ-opioid receptors elicited a large increase in LH release and all 5 ovulated. In contrast, only 3 of 8 rats pretreated with FLA-63 had a large increase in LH release and ovulated, and PBZ prevented the nor-BNI-induced LH increase and ovulation in 4 of 4 rats. PBZ also prevented the afternoon LH surge and ovulation in 4 of 4 rats in our normal colony. Finally, HPLC measurement of NE levels in MPOA push–pull perfusate indicated no increase in NE release during the nor-BNI-induced or normal afternoon LH surges. These results indicate that antagonism of κ-opioid receptors in the MPOA can prematurely evoke an ovulatory LH surge prior to the critical period on the afternoon of proestrus. Furthermore, the nor-BNI-induced as well as the normal afternoon LH surges are dependent on the proper functioning of central noradrenergic neurons, but do not involve increased NE release within the MPOA.

Blockade of ovulation in the rat by systemic and ovarian intrabursal administration of the fungicide sodium dimethyldithiocarbamate

Dithiocarbamates, acting as inhibitors of catecholamine synthesis, have been reported to block ovulation in female rats following systemic administration by suppressing the neural noradrenergic signaling involved in triggering the ovulatory surge of luteinizing hormone. The ovaries also synthesize norepinephrine and receive noradrenergic input via sympathetic innervation, and it has been suggested that such input may play a role in follicular maturation and ovulation. The current experiments investigated whether the dithiocarbamate fungicide dimethyldithiocarbamate (DMDTC) would block oocyte release in normally cycling rats when administered systemically during the proestrous presurge period, and if so, would the compound also have a comparable direct ovarian effect on ovulation in response to a local intrabursal exposure of one ovary late on the day of vaginal proestrus. The results showed that a dose-related suppression of oocyte release was present in response to both intraperitoneal and intrabursal (IB) injections. But these effects appear to be mediated through different mechanisms. The unilateral IB injections were effective only on the exposed side for each ovarian pair, while no alterations were seen in ovarian norepinephrine. IB administration 24 h earlier blocked ovulation on both sides, while hCG injections were able to restore ovulation on the noninjected side only, implying that diestrous DMDTC was inhibiting the LH surge. The data indicate that while an effect on hypothalamic catecholamine synthesis may underlie the ovulatory blockade following intraperitoneal DMDTC administration, it does not appear to be involved in the response to local ovarian exposure. Moreover, the blockade in response to the diestrous IB exposure likely involves two separate mechanisms, one attributable to an alteration in ovarian hormonal feedback to the brain (or pituitary), inhibiting the LH surge, and the other associated with a direct, as yet undetermined, effect on local preovulatory events within the ovary.

Expression of aromatase in the ovary: Down-regulation of mRNA by the ovulatory luteinizing hormone surge

Aromatase (CYP19) mRNA is induced by follicle-stimulating hormone (FSH) in granulosa cells of preovulatory follicles and subsequently is rapidly diminished as a consequence of the luteinizing hormone (LH) surge. Primary cultures of rat granulosa cells were used to identify some of the cellular mechanisms by which FSH increases and LH decreases steady-state levels of aromatase mRNA. Induction of aromatase mRNA by FSH was increased by cycloheximide but was blocked by α-amanitin and the C-kinase activators gonadotropin-releasing hormone (GnRH) and phorbol 12-myristate 13-acetate (PMA). In contrast, the decrease in steady-state levels of aromatase mRNA by LH was mimicked by A-kinase (forskolin) and C-kinase (PMA or GnRH) activators. The decrease in aromatase mRNA was associated with decreased amounts of mRNA and protein for steroidogenic factor-1 (SF-1), a nuclear orphan receptor that binds and trans-activates the aromatase promoter, and with the A-kinase subunit type II (RIIβ), which is required for mediating cAMP action in these cells. The down-regulation of aromatase, SF-1, and RIIβ by each kinase activator and α-amanitin was prevented by cycloheximide when the drug was added in combination with the activator. If, however, cycloheximide was added 2 h after PMA (or LH), the drug did not prevent the rapid loss of mRNA. When granulosa cells were transfected with an aromatase CAT transgene, CAT activity was stimulated 10- to 20-fold by FSH and forskolin but not by PMA. Taken together, these results indicate that the A-kinase but not the C-kinase pathway can trans-activate the aromatase gene in immature granulosa cells, whereas the C-kinase, as well as A-kinase pathways, mimic the LH surge to decrease aromatase mRNA in preovulatory cells. By increasing degradation of aromatase mRNA and by inhibiting transcription, the LH surge rapidly terminates the granulosa cell pattern of gene expression while reprogramming the cells to express genes associated with ovulation and luteinization.

Hormonal regulation of PKC-δ protein and mRNA levels in the rabbit corpus luteum

We have previously reported that rabbit corpora lutea exhibit a prominent phosphorylated substrate protein at 76 kDa which corresponds to the autophosphorylated form of protein kinase C (PKC) δ and that the expression of PKC-δ protein is increased in rabbit corpora lutea of pseudopregnancy at least 2-fold when serum estrogen levels are raised by the presence of an estrogen implant inserted at the time of human chorionic gonadotropin (hCG)-induced ovulation. The purpose of the experiments described herein was to evaluate further the hormonal regulation of PKC-δ in the rabbit corpus luteum. Results demonstrate that luteal PKC-δ protein and mRNA are concomitantly induced some 5-fold within 48 h in response to an ovulatory surge of hCG; that, as in corpora lutea of pseudopregnancy, luteal PKC-δ expression is relatively constant during the life span of the corpus luteum following a fertile mating; that exogenous estrogen does not modulate the induction of luteal PKC-δ during luteinization but promotes an additional two-fold increase in steady state PKC-δ mRNA (and protein) levels in corpora lutea by day 10 of pseudopregnancy; and that luteal PKC-δ expression can be abruptly and reversibly modulated upon withdrawal and subsequent replacement of an estrogen implant to pseudopregnant rabbits. These results demonstrate that an ovulatory surge of luteinizing hormone induces the expression of PKC-δ mRNA and protein in rabbit corpora lutea, and that once the corpus luteum becomes estrogen responsive, estrogen then regulates expression of PKC-δ mRNA and protein.

Immunization of heifers against gonadotropin releasing hormone delays puberty and causes the cessation of estrous cycles

Ten prepubertal Angus X Hereford heifers at 12 months of age were used to determine the effects of primary immunization and booster immunizations against GnRH on ovarian cycles. Five heifers were immunized against GnRH conjugated to human albumin using Freund's complete adjuvant. Booster immunizations against GnRH with Freund's incomplete adjuvant were given in Weeks 6 (B1), 25 (B2) and 46 (B3) after the initial treatment. Progesterone was quantified in blood plasma each week for 68 weeks to assess luteal activity (LA). The initiation of pubertal ovarian cycles occurred at 9.6±1.4 and 20.8±2.4 weeks ( P<0.05) after the primary immunization for control and treated heifers, respectively. Control heifers had normal LA throughout the remainder of the study. Immunization against GnRH did not influence the ovulatory surge of luteinizing hormone after puberty, when titers against GnRH were minimal. Luteal activity ceased in three of five heifers at 1.0±0.6 weeks after B2 and was reinitiated 11.3±0.3 weeks later. After B3, LA ceased in four of five heifers within 3.0±0.7 weeks and was reinitiated 8.2±1.9 weeks later. All heifers became pregnant when exposed to a fertile bull between 100 and 160 days after B3. Immunization of prepuberal heifers against GnRH delayed the initiation of normal ovarian cycles. Booster immunizations against GnRH, after immunized heifers initiated ovarian cycles, caused the cessation of cycles for about 2 months.

Pregnancy Alterations Following Xenobiotic-Induced Delays in Ovulation in the Female Rat

Pregnancy Alterations Following Xenobiotic-Induced Delays in Ovulation in the Female Rat. Cooper. R. L., Barrett, M. A., Goldman, J. M., Rehnberg, G. L., McElroy, W. K., and Stoker, T. E. (1994). Fundam. Appl. Toxicol. 22, 474-480.Chlordimeform [N′-(4-chloro-o-tolyl)-N,N-dimethylformamidine] has been shown to cause a 1-day delay in the surge of luteinizing hormone (LH) in ovariectomized, steroid-primed female rats, presumably through its ability to block CNS α-noradrenergic receptors and consequently CNS regulation of anterior pituitary function. In the present study, we determined whether a chlordimeform-induced delay in the ovulatory surge of LH would alter pregnancy outcome in intact females. Chlordimeform (50 mg/kg) or sodium pentobarbital (35 mg/kg), as a positive control, was administered in order to delay ovulation 24 (1-day delay) or 48 hr (2-day delay). Females were then housed with proven fertile males on the evening of proestrus (0-day delay group), the following evening (1-day delay group), or the evening after that (2-day delay group). The number of receptive females in each group, the mean lordosis quotient, and the number of sperm-positive females in each group were recorded. All females were killed on Gestation Day 20. The number of pregnant females in the 1- or 2-day delay groups was reduced with both chlordimeform and pentobarbital. Also, delaying ovulation for 1 or 2 days with either compound resulted in a significant reduction in the number of live pups present on Gestation Day 20 and a decrease in the number of implantation sites. Litter size was not affected if the females were mated on the same day that treatment was administered (0-day delay). Pentobarbital did not alter the proportion of females showing sexual behavior or the mean lordosis quotient in the 0- and 1-day delay groups, although fewer 1-day females were sperm positive. The number of sexually active and sperm-positive females was reduced in the 2-day pentobarbital-delayed group. However, the lordosis quotient of those that were sexually active was not different than that of control. Similarly, in CDF-treated groups, the proportion of females showing sexual activity was reduced in the 0- and 2-day delayed groups. In contrast, sexual behavior was lower in the 0-day delayed females when tested 2 hr after lights out. These females did eventually mate, however, as confirmed by the high incidence of sperm positive smears the following morning. The number of sperm positive females was lower in both the 1- and 2-day chlordimeform-induced delay groups. Thus, brief exposures to compounds such as formamidine pesticide chlordimeform will result in not only a delay in breeding but, more importantly, a significant reduction in litter size.

Gene expression for estrogen and progesterone receptor mRNAS in rat brain and possible relations to sexually dimorphic functions

A clear neuroendocrine sex difference lies in the ability of the female rat to produce an ovulatory surge of luteinizing hormone. Preoptic neurons, as they respond to estrogen and progesterone, have been proven to be involved in this mechanism, with an emphasis on the possible participation of neurons in the anteroventral periventricular nucleus and the suprachiasmatic portion of the preoptic area (POA). Further, prominent morphological sex differences have been reported in the rat medial POA. To examine expression of the estrogen receptor (ER) and the progesterone receptor (PR) messenger RNAs (mRNAs) in these critical preoptic neurons, we have used in situ hybrization with tritiated single-stranded DNA probes complimentary for ER and PR mRNA. ER mRNA containing cells were found in the periventricular, suprachiasmatic and medical preoptic cell groups, in a manner which agrees with steroid hormone autoradiography. In the female rat, preoptic neurons expressing PR mRNA were distributed very similarly to those for ER mRNA. Moreover, in the male rat brain, all subsets of preoptic neurons which express the PR gene in the female were also detected in the male. Thus, the distribution of PR expressing cells was very similar between females and males. We conclude that the insensivity to the male to progesterone, as regards the hormonal control of ovulation, cannot be due to a total failure of PR gene expression in a specific subset of POA neurons. Instead, male preoptic neurons must be less sensitive to neural or hormonal inducers in the physiological range or perhaps lack sufficient levels of a transcription factor linking progesterone responsive elements to the start sites of hormone-controlled genes.

Steroid control of central neuronal interactions and function

Steroids have potent actions on the brain which can be categorized as; (i) fast (∼ms-s), (ii) intermediate (h-days), (iii) long-term reversible (days-weeks) and (iv) long-term irreversible. Here attention is focussed on the intermediate and long-term reversible effects of steroids with emphasis on glucocorticoids and oestrogen. Glucocorticoid negative feedback is generally classified as fast, delayed and long-term. Fast negative feedback would appear to depend mainly on a reduction in pituitary responsiveness to corticotrophin releasing factor-41 (CRF-41) and possibly arginine vasopressin (AVP). Delayed feedback is mediated by reduced AVP release into hypophysial portal blood and blockade of the ACTH response to CRF-41. Long-term negative feedback is a consequence of reduced CRF-41 and AVP release into portal blood. Lesion and electrical stimulation studies pinpoint the paraventricular nuclei as the main site at which glucocorticoids act to control ACTH release. Oestrogen at physiologically low plasma concentrations inhibits gonadotrophin secretion. At physiologically high plasma concentrations, such as those that occur during the preovulatory surge, oestradiol-17β stimulates the biosynthesis of LHRH mRNA and LHRH and the release of LHRH into hypophysial portal blood. Oestradiol also increases pituitary responsiveness to LHRH. The action of oestrogen on LHRH neurons is probably mediated by interneurons and may involve disinhibition; this view is supported by our in situ hybridization studies which show that oestrogen, in its positive feedback mode, significantly reduces the synthesis of proopiomelanocortin mRNA in arcuate neurons which when active are likely to inhibit LHRH neurons. The mechanism of action of oestrogen on the pituitary gland is not yet established, but clues from the action of the priming effect of LHRH suggests that oestrogen may potentiate phosphoinositide second messenger cascades. LHRH priming involves the synthesis of a 70 kDa protein the N-terminus of which is identical to an oestrogen-induced protein in the ventromedial hypothalamic nucleus involved in lordosis, and to that of phospholipase Cα. Attention is drawn to the remarkable economy of the system by which a single steroid, oestrogen, has effects on the brain and pituitary gland which result in a co-ordinated sequence of amplifier cascades which lead first to the ovulatory surge of luteinizing hormone and then to mating behaviour, both of which are obviously essential for continuation of the species. Long-term reversible effects of steroids are exemplified by (i) the action of testosterone, and its metabolite, oestrogen, in stimulating the synthesis of AVP in neurons of the bed nucleus of the stria terminalis, and (ii) the action of oestrogen in reducing by four-fold the amount of the steroid anaesthetic, alphaxalone, required to induce anaesthesia in the male. These stimulatory and inhibitory actions of glucocorticoids and gonadal steroids on the brain and pituitary gland provide excellent models by means of which the molecular mechanisms of central neurotransmission in mammalian brain can be established.

Melatonin and the ovulatory luteinizing hormone surge

A newly developed 125I-radioimmunoassay allows for the accurate determination of physiological concentrations of plasma melatonin. Melatonin secretion does not change significantly on the day before and the day of the luteinizing hormone (LH) surge when compared with the early follicular phase. In addition, it was confirmed that the beginning of the LH surge frequently occurs in the morning and is associated with low melatonin values (six of nine women). Supraphysiological melatonin concentrations did not decrease the midcycle LH secretion in four women studied.

A Possible Dual Mechanism of the Anovulatory Action of Antiprogesterone RU486 in the Rat1

The purpose of these experiments was to investigate the mechanism of the anovulatory action of antiprogesterone RU486 (RU486) in rats by studying its effects on follicular growth, secretion of gonadotropins and ovarian steroids, and ovulation. Rats with 4-day estrous cycles received injections (s.c.) of either 0.2 ml oil or 0.1, 1, or 5 mg of RU486 at 0800 and 1600 h on metestrus, diestrus, and proestrus. At the same times, they were bled by jugular venipuncture to determine serum concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), 17 beta-estradiol (E), and progesterone (P). On the morning of the day after proestrus, ovulation and histological features of the ovary were recorded. Rats from each group were killed on each day of ovarian cycle to assess follicular development. Rats treated similarly were decapitated at the time of the ovulatory LH surge and blood was collected to measure LH. The serum levels of LH increased and those of FSH decreased during diestrus in rats treated with RU486. Neither E nor P levels differed among the groups. Treatment with RU486 caused both a blockade of the ovulation and an increase in ovarian weight in a dose-dependent manner. At the time of the autopsy (the expected day of ovulation), rats treated with 1 mg RU486 had ovaries presenting both normal and post-ovulatory follicles and unruptured luteinized follicles. Rats treated with 5 mg RU486 presented post-ovulatory follicles without signs of luteinization. The number of follicles undergoing atresia increased in rats treated with RU486. Rats treated with 5 mg RU486 exhibited a significant decrease in ovulatory LH release. The mechanism by which RU486 produces the ovulatory impairment in rats seems to be dual: first, by inducing inadequate follicular development at the time of the LH surge and second, by reducing the amount of ovulatory LH released. The physiological events-decreased basal FSH secretion and follicular atresia-that result from use of RU486 cannot be elucidated from these experiments and should be investigated further.

In situ hybridization for LHRH mRNA following estrogen treatment

Elucidation of mechanisms governing the synthesis and release of the decapeptide luteinizing hormone-releasing hormone (LHRH) in the female are central for understanding how the brain influences the ovulatory surge of luteinizing hormone and facilitates female rat mating behavior. Previous immunocytochemical results suggested that estrogen treatment might increase LHRH forebrain content, but measures of peptide content often are confounded by alterations in synthesis versus peptide processing versus release. Therefore, we have used in situ hybridization with an oligomer for the LHRH coding region to detect LHRH gene expressing cells and to study LHRH message levels in estrogen treated compared to control ovariectomized rats. Neurons expressing the gene for LHRH are in the medial preoptic area and amongst the fibers of the diagonal bands of Broca. When the numbers of neurons with detectable LHRH message levels were multiplied by the average numbers of grains per cell, to achieve a metric proportional to LHRH message content, we saw a significant stimulatory effect of seven days of estrogen treatment.

Blood LH level and induced ovulation after hCG and PMSG treatment in ovarian quiescent cattle.

Ovarian quiescent cattle bearing follicle with palpable size were treated with single intramuscular injection of 750-6,000 IU of human chorionic gonadotrophin (hCG) in 13 cases and 1,000-2,000 IU of pregnant mare serum gonadotrophin (PMSG) in 5 cases. Changes of blood luteinizing hormone (LH) level, estrus and ovulation after the treatments were examined. After the hCG treatment LH level became slightly high from 0.2-0.6 ng/ml of pre-treatment to 0.3-1.9 ng/ml of post-treatment and maintained the level up to ovulation without the ovulatory LH surge. Ovulation was induced about 36 hr after the treatment in 12 cases. The ovulations were all silent ovulations. After the PMSG treatment LH level became slightly high from 0.6 ng/ml of pre-treatment to 1.3 ng/ml of post-treatment and the level lasted until the ovulatory LH surge. The ovulatory LH surge occurred about 39 hr after the PMSG treatment in 4 cases with a peak of about 32 ng/ml. Ovulation was induced about 74 hr after the treatment in all 5 cases. Four cases showed estrus but one in which the LH surge could not be confirmed did silent estrus preceding the induced ovulations. It was demonstrated that hCG induced ovulation without the LH surge but PMSG induced the ovulatory LH surge and the subsequent ovulation in ovarian quiescent cattle.

Endocrine regulation of the corpus luteum.

The corpus luteum is a small gland that develops rapidly from the ovulated follicle and performs a vital function in the reproductive process, namely, the secretion of progesterone, which is necessary for implantation of the blasto­ cyst. Following implantation, the continued secretion of progesterone is essential to maintain a quiescent uterus and an intrauterine environment that is conducive to continued development of the embryo (29). If fertilization or implantation does not occur, the corpus luteum regresses, and the consequent withdrawal of progesterone leads to increased frequency of pulsatile luteiniz­ ing hormone (LH) secretion, increased follicular estrogen synthesis, and a new follicular phase (56). If implantation occurs, then the embryo signals the corpus luteum either directly or indirectly to continue to secrete progesterone and to prevent the corpus luteum from regressing (78). Thus, the corpus luteum can be viewed as the terminal stage of the ovarian follicle, which after shedding the oocyte, continues to nurture the (fertilized) egg indirectly by producing progesterone. The progestational changes in the uterus must pre­ cede the arrival of the preimplantation embryo and require the rapid conver­ sion of the predominantly estrogen-producing follicle to a predominantly progesterone-producing corpus luteum. This is accomplished by the pre­ ovulatory surge of luteinizing hormone, which serves the dual role of stimulating both ovulation and the conversion of the follicle into a corpus luteum, a process known as luteinization (57). This review COncentrates On certain aspects of the regulation of the corpus luteum that represent relatively new directions in research, and emerging concepts. For more information about the regulation of the corpus luteum in

Changes in local cerebral glucose utilization associated with the spontaneous ovulatory surge of luteinizing hormone in the rat.

Brain activity during the spontaneous ovulatory surge of luteinizing hormone (LH) has been studied by measuring local cerebral glucose utilization (LCGU) by the [14C]-2-deoxyglucose method. The LCGU was determined in 37 brain areas and the pituitary gland in conscious, freely moving female rats in the morning and the late afternoon of proestrus. No increases in LCGU were detected, but, unexpectedly, there was a significant decrease in the LCGU measured in the afternoon compared with the morning of proestrus in the medial preoptic and anterior hypothalamic areas, the arcuate nucleus, median eminence and amygdala. Significant reductions in LCGU also occurred in the midbrain central grey and reticular formation. These results suggest that the LH and/or the prolactin surge is associated with a significant reduction in the activity of brain areas known to be essential components of the central control of gonadotropin and prolactin secretion. In the case of the arcuate nucleus and median eminence, for example, the results could be explained by a decreased activity of the opioid and dopaminergic neurons which are known to inhibit the release of luteinizing hormone releasing hormone (LHRH). Disinhibition of LHRH neurons would result in the increased release of LHRH into the hypophysial portal vessels. Reduction in the activity of the arcuate dopamine neurons could also play a major role in the prolactin surge. The decreased LCGU of the midbrain central grey may be related to the onset of lordosis behavior which appears to be time-locked to the LH surge.

The effect of PMSG on ovarian function in ovarian quiescent heifers.

Twenty Holstein heifers with ovarian quiescence were assigned to 4 treatment groups. Heifers of Groups I (n=6), II (n=6), III (n=5) and IV (n=3) were treated with a single intramuscular injection of 500, 1, 000, 2, 000 and 4, 000 IU of PMSG, respectively. Ovarian changes were inspected by rectal palpation after the treatment. Changes of plasma estradiol-17β(E2) and progesterone (P) levels in the peripheral blood plasma were examined by radioimmunoassay in 5 of the heifers. E2 level increased sharply and reached a peak 2 days after the treatment. 0vulation was induced 2-4 days after the treatment in 18 heifers (90%) except in 2 heifers of Group I. Three types of corpus luteum (CL) developed after the induced ovulation: hypoplastic and short-lived, well developed but short-lived, and well developed and normal life-spanned. The CL were accompanied by an obvious elevation of blood P level. Second ovulation occurred spontaneously in 6 heifers (30%) 8-22 days after the induced ovulation. Many follicles grew in some heifers of Group II and most heifers of Groups III and IV, accompanied by high E2 peak on the 7th day of posttreatment. It was indicated that PMSG stimulated the growth, maturation and active E2 secretion of follicle and induced the ovulation in ovarian quiescent heifers. It was suspected too that the increased E2 triggered the ovulatory luteinizing hormone surge so that ovulation occurred subsequently.

Chapter 15 Functional recovery from neuroendocrine deficits: studies with the hypogonadal mutant mouse

This chapter discusses the effect on the reproductive physiology of the hypogonadal male host of grafts, containing GnRH cells that were obtained from a region not known to project to the median eminence, and the effect of preoptic area grafts placed in the lateral ventricle far from the median eminence. The chapter also presents measurement of plasma luteinizing hormone (LH) in relation to mating in hypogonadal females with preoptic area grafts to determine the presence of an ovulatory LH surge in mutant animals with preoptic area grafts. The ability of preoptic area grafts to correct deficiencies in reproductive development is an important example of successful neural transplants, demonstrating that grafted neuropeptide-secreting cells may survive, develop axonal projections into the appropriate region of the host brain, and secrete their products in a physiological manner. Graft tissue derived from neonatal mouse brain appears to result in as frequent and vigorous correction of reproductive deficiencies as does tissue derived from fetal brain. Anatomical studies confirm that there are synapses onto gonadotropin hormone-releasing hormone (GnRH) perikarya and dendrites within the grafts, although whether the source is intrinsic or extrinsic to the grafts is not yet defined.

The role of ovine conceptus secretory proteins in the establishment of pregnancy.

Sheep (Ovis aries) that are not pregnant have recurring estrous cycles of about 17 days’ duration during the breeding season, i.e., August through December to January. The first day of behavioral estrus is designated Day 0 with ovulation occurring about 30h after onset of estrus and the ovulatory surge of Luteinizing Hormone (LH). The estrous cycle is characterized by growth (Days 4–12) and then regression (luteolysis) of the corpus luteum (CL). Luteolysis begins on about Day 15 after onset of estrus. Prostaglandin F2-alpha (PGF), produced by the uterine endometrium, is the uterine luteolytic hormone in sheep (1). Beginning on Days 14 to 15 and continuing until the onset of the next period of estrus, PGF is released in a pulsatile manner. About 5 episodes of PGF release per 24h are required for luteolysis (2,3).KeywordsCorpus LuteumEstrous CycleUterine HornOxytocin ReceptorUterine EndometriumThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.