Serum cholesterol and triglycerides in postpartum beef cows and their relationship to the resumption of ovulation

The variations in lipid metabolism according to the physiological stage and their relationship to the resumption of postpartum ovarian cyclicity were assessed in Limousine beef cows fed a grass diet over 3 yr. Weekly blood samples were collected from 59 cows beginning 10 wk before to 20 wk after calving to evaluate serum cholesterol and triglyceride concentrations and electrophoretic lipoprotein fractions. After parturition, progesterone concentrations were also measured at weekly intervals to determine time of resumption of ovulation. Cows were categorized by resumption of postpartum ovarian cyclicity into 3 groups: early (4 to 6 wk post partum, n = 36); mid (7 to 10 wk post partum, n = 46) and late (after 11 wk post partum, n = 38). Higher serum triglyceride values (P<0.05) were observed during the last 10 wk of pregnancy (0.36+/-0.15 g/L) than during the first 20 wk of suckling (0.29+/-0.09 g/L). Cholesterol values decreased significantly (P<0.05) at the end of pregnancy, were minimal (1.01+/-0.03 g/L) at parturition, and increased again up to 9 wk post calving. Increased cholesterolemia and low serum triglyceride values after calving could be linked to the increased bovine alpha-lipoprotein fraction and decreased beta fraction. Serum triglyceride concentrations were not related to the resumption of postpartum ovarian cyclicity. Higher serum cholesterol values were observed from 2 wk before to 4 wk after calving in cows with early rather than mid and late resumption of ovarian cyclicity. Therefore, modifications in lipid metabolism during the puerperium seem to be related to resumption of cyclicity during the early postpartum period.     

Alterations in hypophysial responsiveness to synthetic GnRH at different postpartum intervals in Murrah buffalo (Bubalus bubalis )

The objective of this study was to investigate the hypophysial responsiveness to GnRH at different intervals post partum in Murrah buffalo. Plasma LH and FSH levels were measured at 1 h before and upto 6 h subsequent to the administration of GnRH (1 ug/kg body weight) or saline on Days 2, 20 and 35 post partum in 2 groups of buffalo (n=4 each). Plasma progesterone levels were measured in samples collected once daily from Day 3 to Day 46 post partum. Pretreatment basal LH levels exhibited a progressive increase from Day 2 through Day 35 post partum, while the basal FSH levels increased only until Day 20 post partum. Following a highly subdued LH response to GnRH on Day 2 post partum, a 408% increase (P < 0.01) was observed in the total LH released in response to GnRH on Day 20 post partum, followed by a 20% reduction (non-significant) over Days 20 to 35 post partum. The interval from parturition was highly correlated with total LH released (r = 0.711, P < 0.01). Unlike LH, a substantial amount of FSH was released following GnRH treatment on Day 2 post partum, which was not significantly different from the FSH response on Days 20 and 35 post partum. The LH and FSH response to GnRH was not significantly different between animals in which luteal activity resumed and in those which showed no luteal activity post partum. While pointing to a dramatic enhancement in the hypophysial responsiveness to GnRH between Days 2 and 20 post partum, these results suggest that pituitary responsiveness to GnRH does not appear to be the limiting factor for resumption of estrous cycles by Day 35 post partum in Murrah buffalo.     

Plasma progesterone and gonadotrophin concentrations and ovarian activity in post-partum dairy cows

Plasma progesterone concentrations in jugular vein blood samples collected every other day after calving from 13 Friesian dairy cows indicated that ovarian cyclic activity was initiated by 16.6 +/- 1.1 (s.e.m.) days post partum, except for 1 cow which did not resume cyclic activity until Day 98 post partum. Rectal palpation of the ovaries indicated that a developing follicle was recognizable at a mean time of 15.7 +/- 2.0 days after calving. During the first oestrous cycle after parturition there was a significantly shorter period when plasma progesterone levels were elevated than during the next 2 cycles. Concentrations of progesterone, LH, FSH and prolactin were determined for 4 cows, in blood samples taken every 6 h from 2 to 36 days post partum. Tonic LH release was lower during the first 10 days than subsequently, but the lack of change in pattern for FSH suggests dissimilar control mechanisms for these hormones during this time. Three cows showed evidence of a resumption of ovarian cyclicity during the sampling period: in 2 there was an initial LH surge of a magnitude which would normally give rise to ovulation, followed 4 days later by an increase in plasma progesterone lasting only 5 and 9 days. This progesterone was considered to be of follicular origin. A second LH surge was followed by the presence of a corpus luteum.     

Down regulation of prolactin receptors in the hamster ovary by the preovulatory gonadotropin surge

Binding of 125I-prolactin (Prl) to hamster ovarian homogenates was found to decrease markedly at the time of the preovulatory gonadotropin surge (PGS). Saturation analysis revealed that the decrease was due to a reduction in the number of available Prl receptors and not due to a change in binding affinity. Loss of Prl receptors following the PGS was not affected by treatment with ergocryptine to block the release of pituitary Prl, indicating that the reduction in the number of available Prl receptors was not due to increased occupancy by endogenous Prl. Loss of Prl receptors was prevented by treatment with phenobarbital (Phen) to block the normal luteinizing hormone (LH)/follicle-stimulating hormone (FSH) surge; whereas, an injection of 50 micrograms of LH or 50 micrograms FSH (but not 100 micrograms Prl) induced a marked decrease in Prl receptors in Phen-treated hamsters. To determine whether Prl receptor loss induced by 50 micrograms FSH might be due to LH contamination, Phen-treated hamsters were injected with minimal ovulatory doses of LH and FSH. Injection of 5 micrograms or 2.5 micrograms LH induced a loss of Prl receptors in 90% and 70% of Phen-treated hamsters, respectively. In contrast, injection of 5 micrograms or 2.5 micrograms FSH induced a loss of Prl receptors in 0% and 20% of Phen-treated hamsters, respectively. These results indicate that the PGS causes an acute heterologous down regulation of ovarian Prl receptors and suggest that this down regulation may be due principally to the action of LH.     

Developmental programming: exogenous gonadotropin treatment rescues ovulatory function but does not completely normalize ovarian function in sheep treated prenatally with testosterone

Prenatal testosterone treatment leads to LH excess as well as ovarian follicular and ovulatory defects in the adult. These disruptions may stem from LH excess, abnormal FSH input, compromised ovarian sensitivity to gonadotropins, or intrinsic ovarian defects. To determine if exogenous gonadotropins rescue ovarian and ovulatory function of testosterone-treated sheep, the release of endogenous LH and biopotent FSH in control and prenatal testosterone-treated sheep was blocked with a GnRH antagonist during the first two breeding seasons and with LH/FSH coadministered in a manner approximating natural follicular phase. An acidic mix of FSH was administered the first 36 h at 2-h intervals and a less acidic mix for the next 12 h at 1-h intervals (different FSH preparations were used each year), and ovulation was induced with hCG. Circulating FSH and estradiol responses to gonadotropins measured in 2-h samples differed between treatment groups in Year 1 but not in Year 2. Ovarian follicular distribution and number of corpora lutea (in ewes that ovulated) tracked by ultrasonography and luteal progesterone responses were similar between control and prenatal testosterone-treated females but differed between years. Furthermore, hCG administration induced large cystic and luteinized follicles in both groups of females in Year 2, although the growth rate differed between control and prenatal testosterone-treated females. Our findings provide evidence that 1) ovulatory response in prenatal testosterone-treated females can be rescued with exogenous gonadotropins, 2) resultant follicular response is dependent on the nature of gonadotropic input, and 3) an abnormal follicular milieu may underlie differences in developmental trajectory of cystic follicles in prenatal testosterone-treated females.     

Resumption of gonadotrophin release during the post-partum period in suckling and non-suckling ewes

The post-partum secretion of LH, FSH and prolactin was monitored in 15 suckling and 6 non-suckling Préalpes du Sud ewes lambing during the breeding season by measuring plasma hormone concentrations daily at 6-h intervals and also weekly at 20-min intervals for 6 h from parturition to resumption of regular cyclic ovarian activity. There was a constant phenomenon in the resumption of normal patterns of FSH and LH secretion: there was a rise in FSH values culminating on average on Day 4 post partum and returning subsequently to values observed during the oestrous cycle, and concurrently an increase in the frequency and amplitude of LH pulses more progressive in suckling than in non-suckling ewes which led to an elevation of LH mean concentrations and occurrence of an LH surge. Since neither the FSH secretory pattern nor FSH mean values differed between suckling and non-suckling ewes, the results suggested that LH pulsatile pattern was a major limiting factor for the resumption of normal oestrous cycles. Before regular oestrous cycles resumed other changes in preovulatory LH surges also occurred: (i) they increased in duration and probably in amplitude; (ii) they were preceded by an acceleration in LH pulse frequency and a large decrease in FSH values as in normal cyclic ewes; and (iii) at least in non-suckling ewes they occurred concurrently with a prolactin surge.     

Binding of high-density lipoproteins to luteal membranes: the role of prolactin, luteinizing hormone, and circulating lipoproteins

Ovarian and adrenal membranes from immature gonadotropin-primed rats, treated with 4-amino-pyrazolopyrimidine (4APP) to reduce endogenous lipoprotein levels, displayed higher binding of porcine high-density lipoprotein (HDL) when compared to control rats. Immature, hypophysectomized (HYPOX) rats bearing corpora lutea (CL) on Day 5 after ovulation had lower levels of serum progesterone and reduced capacity for HDL and human chorionic gonadotropin (hCG) binding to ovarian membranes when compared with intact animals. Hypophysectomy also reduced the number of HDL binding sites in adrenal membranes. Treatment of HYPOX animals with luteinizing hormone (LH) and prolactin (Prl) alone or in combination increased the HDL binding sites in the ovary relative to HYPOX-untreated rats. Neither hormone affected binding to adrenals, where only adrenocorticotropic hormone (ACTH) enhanced HDL binding. LH treatment reduced the serum progesterone levels and hCG binding to the ovaries, whereas Prl administration increased progesterone levels with no effect on hCG binding. We conclude from this study that HDL binding in the luteinized ovary is regulated by Prl and LH and circulating lipoproteins, whereas in adrenals it is regulated by ACTH and circulating levels of lipoproteins.     

Role of the corpus luteum of pregnancy in controlling pituitary gonadotrophin secretion during the early post-partum period in the ewe

No difference was found between 5 intact ewes and 5 ewes from which the CL had been excised at Day 70 of pregnancy in the plasma concentration of progesterone at Day 140, and concentrations of progesterone remained below 0.2 ng/ml during the first 20 days post partum. Plasma concentrations of LH, frequency and amplitude of LH pulses were low at Day 140 and increased considerably, particularly in the CL-excised ewes, as early as Day 5 post partum. No significant differences were found between the two groups of ewes in the mean plasma concentrations of FSH for any of the 5 stages examined. Taken together, these results suggest that some factor, other than progesterone, associated with the CL of pregnancy is involved in the inhibition of pulsatile LH secretion during the early post-partum period.     

Gonadotropin levels in ovarian cyst fluids: a predictor of malignancy?

Gonadotropins can stimulate ovarian cancer growth in cell cultures. Corresponding LH/hCG receptors have been demonstrated in ovarian cancer. However, reduction of elevated serum gonadotropins by GnRH analogs in ovarian cancer patients did not lead to growth restriction, which means that serum levels of gonadotropins may not play the most important role in ovarian cancer. We therefore analyzed the LH and FSH concentrations in cyst fluids of ovarian cancer. Patients with preoperatively diagnosed cystic ovarian tumors were eligible for the study. Serum samples of the patients were obtained during surgery, while the fluids within the cysts were aspirated after surgical removal of the tumor. FSH and LH levels in serum and cyst fluids were measured using single antibody EIA (Boehringer Mannheim GmbH, Germany). Cyst fluids and sera of 108 patients were evaluated. While there were no significant differences in the FSH and LH serum concentrations, highly significant differences in the FSH and LH levels in cyst fluids were found. Only cancer cysts contained FSH and LH, while the corresponding concentrations in benign cysts were always below the measuring range of the assays. This clear division between high gonadotropin levels in cysts of serous ovarian cancer and low or absent concentrations in benign ovarian tumors further supports the hypothesis that FSH and LH may play a role in ovarian cancer; however, explanations for this surprising finding are still lacking.     

Postpartum acyclicity in suckled beef cows: a review

Prolonged postpartum acyclicity in suckled beef cows is a source of economic loss to beef cattle producers. Duration of postpartum acyclicity is influenced by suckling status, nutritional status, calving season, age, and several other factors. Although uterine involution begins and ovarian follicular waves resume soon after parturition, dominant follicles of these waves fail to ovulate, due to a failure to undergo terminal maturation. As a result, postpartum anovulatory dominant follicles are smaller than the ovulatory follicles in cyclic cows. Failure of postpartum dominant follicles to undergo terminal maturation is due to absence of appropriate LH pulses, a prerequisite for follicular terminal maturation prior to ovulation. Absence of LH pulses early post partum is primarily due to depletion of anterior pituitary LH stores, although GnRH pulses are also absent during this period due to suckling. Following replenishment of LH stores between Days 15 and 30 post partum, absence of LH pulses is due to continued sensitivity of the hypothalamic GnRH pulse-generator to the negative feedback effect of ovarian estradiol-17beta, which results in absence of GnRH pulses. This negative feedback effect of estradiol-17beta is modulated by suckling which stimulates release of endogenous opioid peptides from the hypothalamus. As the postpartum interval increases, sensitivity of the GnRH pulse-generator to the negative feedback effect of ovarian estradiol-17beta decreases. This is followed by an increasing frequency of GnRH discharges and LH pulses, terminal follicular maturation, ovulation, and continued cyclicity. The first ovulation post partum is usually followed by a short cycle due to premature luteolysis because of premature release of PGF2alpha from the uterine endometrium, which is possibly intensified by the suckling-induced oxytocin release from the posterior pituitary. A model for the postpartum ovulatory acyclicity and for the resumption of cyclicity is presented.     

Influence of ovaries and photoperiod on reproductive function in the mare.

A 16 h daily photoperiod hastened the onset of the ovulatory season (first ovulation); gonadotrophin and follicular changes prior to the onset were similar in intact light-treated and control mares. A preovulatory decline in FSH concentrations before the onset of the ovulatory season preceded the decrease in number of follicles (15--25 mm) and the rise in LH concentrations which was temporally associated with the growth of an ovulatory follicle. Seasonal changes of FSH and LH concentrations were found in ovariectomized mares and were influenced by photoperiod. During the anovulatory season, there was no ovarian influence on gonadotrophin concentrations. However, during the ovulatory season the ovaries exerted a positive influence on seasonally elevated LH concentrations during oestrus and a negative influence during dioestrus. The ovaries exerted a negative influence on seasonally elevated FSH concentrations throughout the oestrous cycle. The onset of the ovulatory season occurred at the time of the first sustained increase in LH concentrations resulting from positive seasonal (increasing photoperiod) and ovarian influences.     

A possible dual mechanism of the anovulatory action of antiprogesterone RU486 in the rat

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.     

Evolutionary and Functional Aspects of Pituitary Gonadotropins in the Green Turtle, Chelonia Mydas

Information on the pituitary gonadotropins in Chelonia mydasrepresents some of the most complete data available for anyreptile and thus provides an important basis for evaluatingevolutionary processes in tetrapod endocrine physiology. Thetwo gonadotropins isolated from Chelonia pituitary glands showclear chemical and immunological homologies to mammalian follicle-stimulatinghormone (FSH) and luteinizing hormone (LH). However, receptorstudies and biological tests indicate that the functions ofthese hormones may be different in turtles and mammals. In particular,Chelonia LH shows an unusual ability to interact with FSH receptorsites and to stimulate physiological functions normally attributedto FSH. Results with Chelonia LH demonstrate that errors mayarise from using mammalian hormones to investigate reproductionin turtles. Measurements of endogenous gonadotropin levels inthe plasma of breeding and nesting Chelonia provide a differentperspective of the potential roles of the FSH and LH from thatobtained in physiological tests. In particular, FSH and LH secretionare markedly dissociated during the nesting cycle; FSH has onlya transient peak during oviposition, whereas LH, along withprogesterone, displays a pronounced "ovulatory" surge in theday following nesting. Preliminary studies with synthetic gonadotropicreleasing factors in Chelonia suggest that these may be usefulin inducing reproductive changes.     

Seasonal effects on ovarian folliculogenesis in rhesus monkeys

Reproductive performance is reportedly reduced in some rhesus monkeys during the summer months, even when environmental conditions are controlled. The mechanism(s) underlying this phenomenon remain unknown. We noted that the pattern of folliculogenesis appeared to be altered in rhesus monkeys that continued to exhibit ovulatory menstrual cycles during the "nonbreeding" season. This study was designed to investigate the effect of season on development of the dominant follicle (DF) and upon levels of serum gonadotropins and sex steroids in animals maintained in a controlled environment. Forty-four menstrual cycles were evaluated from October, 1982 to October, 1983. Animals were housed individually in controlled light (12L:12D) and temperature (22-25 degrees C). A DF was identified by laparoscopy on Day 6 of the cycle in only 45% of cycles during the months of May through September, compared with 87.5% the remainder of the year. No effect of season was detected on either the length of the menstrual cycle or luteal phase, mean follicular diameter, or the percentage of ovulatory cycles. During the follicular phase, amounts of follicle-stimulating hormone (FSH) in peripheral sera were depressed, whereas those of luteinizing hormone (LH) were consistently elevated. Amounts of circulating estradiol were similar between groups. However, serum concentrations of progesterone were markedly reduced in the summer. Development of the DF appeared to be delayed in the early follicular phase during the summer months in those rhesus monkeys that had ovulatory menstrual cycles. This delay was accompanied by an alteration in the FSH to LH ratio. Although most cycles were ovulatory, altered follicular development resulted in deficient luteal function.     

Changes in gonadotrope responsivity to gonadotropin releasing hormone during development of the rhesus monkey

To assess the changing responsiveness of pituitary gonadotropes to gonadotropin releasing hormone (GnRH) during development, 5 male and 5 female rhesus monkeys were studied. Three monkeys of each sex were tested periodically with a subcutaneous injection of 500 micrograms of GnRH dissolved in 50% polyvinylpyrrolidone (PVP) beginning at 2 to 4 weeks of age and continuing into young adulthood. The remaining 4 monkeys received injections of the vehicle (PVP) alone and served as controls. Serum concentrations of bioactive luteinizing hormone (LH) were determined by an interstitial cell testosterone bioassay, and follicle-stimulating hormone (FSH) levels were measured by radioimmunoassay. Baseline FSH levels in the 5 female neonatal monkeys were higher than those of the 5 male neonatal monkeys during the first 2 months of life. In both sexes, FSH concentrations decreased with age, and FSH was barely detectable by 6 months. Baseline LH values in the 5 female monkeys declined during the first 6 months of the study and were undetectable (less than 0.5 micrograms/ml) at 6 months of age. Baseline LH levels in 4 of the 5 neonatal males also declined to undetectable concentrations by 6 months of age. During the first 3 months of life, there was a striking increase in the serum concentrations of both LH and FSH following GnRH. Although the LH responses to GnRH (delta LH) were similar in males and females of comparable ages, the FSH responses (delta FSH) were considerably greater in the female monkeys. In the males, the delta LH exceeded the delta FSH, whereas in the females, the delta FSH were greater than the delta FSH. In both sexes, the delta LH and delta FSH generally were greatest in the youngest monkeys and decreased gradually with increasing age. By 6 months, the gonadotropin responses to GnRH either were undetectable (males) or very small (females). After 6 months there was no longer an increase in serum gonadotropins after GnRH in either sex until 1.5-4 years (females) or 3 years (males) of age. The delta LH in response to GnRH in the male monkeys 3-5 years of age were comparable to the responses during the first month after birth. Serum concentrations of FSH in the adult males, however, did not increase after GnRH. In the female monkeys, serum levels of LH and FSH increased after GnRH at 1.5 years (1 monkey) and 4 years (2 monkeys) of age. The delta LH were similar to those of the 1- to 2-month-old female monkeys. The delta FSH, however, were variable and were approximately 20% of the neonatal response. In these young adult female monkeys the delta LH exceeded the delta FSH.(ABSTRACT TRUNCATED AT 400 WORDS)     

Immunoreactive inhibin levels in peripheral blood during the breeding season in the female Japanese monkey

Serum levels of immunoreactive inhibin as well as FSH, LH, estradiol-17 beta, and progesterone were measured by RIA in four mature female Japanese monkeys (Macaca fuscata fuscata) during the breeding season and subsequent transition into the nonbreeding season. During the breeding season, each monkey showed 2-6 ovulations, which were inferred from underlying endocrine events. The concentrations of serum inhibin increased during the luteal phase, but were low during the follicular phase. Such changes in serum inhibin levels correlated positively with those in serum progesterone levels. Basal levels of serum inhibin also increased during the breeding season, decreased during transition from the breeding season, and were low during the nonbreeding season. The parallel change in serum levels of inhibin and progesterone together with the increased basal levels of serum inhibin during this period suggests that both the CL and antral follicles are sources of circulating inhibin. Decreases in serum FSH levels during the luteal phase suggest that secretion of FSH is controlled by an inhibitory action of ovarian inhibin in addition to steroid hormones.     

Gonadotropin secretion during prolonged hyperprolactinemia: basal secretion and the stimulatory feedback effect of estrogen

Inoculation of cyclic female rats with the prolactin (Prl)/growth hormone-secreting pituitary tumor, MtT.W15, resulted in a cessation of estrous cyclicity within 5--10 days. Associated with this acyclicity was a persistently low serum concentration of estradiol and marked increases in both circulating Prl and progesterone. At Day 26 of acyclicity, basal serum luteinizing hormone (LH) values measured in samples taken every 20 min from 0900--1100 h were significantly reduced when compared to cyclic, nontumor animals on diestrus Day 2. There was no difference in basal follicle-stimulating hormone (FSH) concentrations. In a separate group of acyclic, tumor-bearing females 42--56 days after transplantation, a single s.c. injection of 20 micrograms estradiol benzoate (EB) at 1030 h elicited significant increases in both serum LH and FSH values between 1700 and 1830 h on the next day. The magnitude of the LH surge was reduced and that of FSH was increased in tumor-bearing animals when compared to cyclic, nontumor females given a similar EB injection on diestrus Day 1. These results demonstrate that chronic hyperprolactinemia is associated with inhibition of basal LH secretion and ovarian estrogen production and an increase in circulating progesterone concentrations. Nevertheless, the stimulatory feedback effects of estrogen on LH and FSH release are still present and functioning in acyclic female rats under chronically hyperprolactinemic conditions. These data suggest that the cessation of regular ovulatory cycles associated with hyperprolactinemia may be due to a deficiency of LH and/or estrogen secretion, but not to a lack of central nervous system response to the stimulatory feedback action of estrogen.     

Central effects of an antagonist and an antiserum to substance P on serum gonadotropin and prolactin secretion

The central effects of both an antagonist and an antiserum to substance P (SP) on gonadotropin and prolactin (Prl) secretion were studied in castrated male rats. The lateral ventricular injection (20 micrograms) of an analogue to SP possessing antagonistic properties resulted in significantly suppressed serum LH levels without altering serum FSH and Prl levels when compared with saline-injected control animals. Similarly, the lateral ventricular injection of an antiserum to SP also resulted in significantly suppressed LH levels when compared to control animals injected with normal rabbit serum. Additionally, no changes were observed in the levels of serum FSH and Prl as a result of the anti-SP injection. Thus, although indirect, these results support the hypothesis that SP may have a central stimulatory action on LH secretion, but not FSH and Prl secretion.     

Serum lipoproteinemia in pregnant and lactating rats

Serum lipoproteins of pregnant and puerperal rats were studied by preparative and analytical ultracentrifugation. The concentration for the fraction with density less than 1.019 was markedly elevated in rats during the 3rd wk of gestation and in lactating rats. This fraction showed similar triglyceride fatty acid composition and immunoelectrophoretic behavior whether it was derived from pregnant or nonpregnant rats, and when partially delipidized, the lipoproteins from both groups showed similar immunoelectrophoretic characteristics and sedimentation rates. When lactation was interrupted during puerperium, serum lipoproteins returned to control levels; but in lactating rats, high levels of serum very low density lipoprotein persisted up to 3 wk post partum.     

Effects of ovariectomy on clock-timed daily gonadotropin rhythms in prepubertal golden hamsters

Daily rhythms of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) are measurable in the serum of prepubertal female golden hamsters by 17 days after birth. These rhythms, which are characterized by peak levels at 1700 h, persist until they are replaced by a 4-day rhythm as ovulatory cycles begin, approximately 3 wk later. We have tested the proposition that the ovaries are required for the onset and maintenance of clock-timed gonadotropin release by removing the ovaries and measuring the levels of LH and FSH in prepubertal hamsters. Ovariectomy was performed both before and after the onset of the rhythm and the effect of removal was determined by subsequent collection of blood samples during the mid- to late-prepubertal period. Ovariectomy on 7, 10 or 13 days after birth results in tonic levels of LH and FSH in blood samples collected at 1400, 1700 and 2000 h on Days 17 through 29. Sham-operated or intact controls had significantly elevated levels of these hormones at 1700 h. Ovariectomy on Day 21 and killing on Day 25 at the same times of day abolished the rhythm of serum LH measured in sham-ovariectomized controls. Ovariectomy on Day 21 and killing on Days 26, 28 or 30 at hourly intervals resulted in variable but nonrhythmic patterns of circulating LH. Thus, ovariectomy before the initiation of clock-timed gonadotropin release prevented its initiation; ovariectomy after its initiation abolished the rhythm. These results show that the ovary provides an essential "message" to the brain-pituitary axis for the initiation and maintenance of clock-timed gonadotropin release in prepubertal females.