Basal Prolactin Concentrations Research Articles

THE PROLACTIN RESPONSE TO SUCKLING

Changes in prolactin concentration during single suckling episodes in twenty breast-feeding women from four to 40 weeks post partum have been investigated. Basal prolactin concentration and the increase in prolactin secretion in response to single suckling episodes and amount of milk taken by the infant were both independent of time post partum until the introduction of supplementary feeds, when a significant decrease with time was apparent. Basal concentrations of prolactin were dependent upon the interval between suckling episodes, and the magnitude of the prolactin response varied with the time of day when suckling took place. The relationship between acute suckling episodes and the long term pattern of prolactin secretion over time post partum is discussed.

Inhibition of prolactin secretion by moderate and high doses of testosterone.

The effects of different doses of testosterone on basal and stimulated secretion of prolactin (PRL) were investigated. Intact female mice of the S/W strain were injected sc with 0, 1, 10, 20, 50, 250, 500, 1000, 2500, or 5000 micrograms of testosterone propionate (TP) once daily for 4 weeks. Serum testosterone concentrations of TP injected mice rose 2- to 5-fold above those of controls at 1- to 50-micrograms doses, and 25- to 600-fold over controls in mice given higher doses of the steroid. Administration of 1 microgram of TP, the lowest dose tested, had no significant effects on basal serum PRL concentrations and only slightly inhibited the release of PRL induced by perphenazine, but the weight and PRL concentration of the pituitary gland were significantly depressed. However, at doses of 10, 20, and 50 micrograms TP, perphenazine-induced PRL release, pituitary PRL concentration, and pituitary gland weight were all reduced in a dose-related manner. The basal serum PRL concentrations decreased by the time the dose of TP reached 50 micrograms. In contrast, higher doses of TP (250 micrograms and above) reversed the suppression of these parameters: pituitary gland weight and basal serum PRL levels were restored to control levels, whereas pituitary PRL concentrations and perphenazine-induced PRL release were partially restored. These results suggest that administration of moderate and large doses of testosterone may suppress natural episodic and acute releases of PRL.

Calcitonin treatment and plasma prolactin levels in pregnant and lactating ewes.

The intravenous injection of a physiological dose of salmon calcitonin (0.5 microgram/kg bw) in 5 ewes on day 125 of gestation induced a slight but significant hypocalcaemia. It had no significant effect on plasma prolactin levels. Ten days after parturition the same dose of salmon calcitonin given in a similar manner to 5 ewes has no effect on suckling-induced prolactin release, although it significantly decreased plasma calcium concentration. This demonstrates that short-term changes in plasma calcitonin concentration have no effect on basal plasma prolactin concentration or on suckling-induced prolactin surge in ewes.

Gamma-aminobutyric acid is not likely a physiological prolactin-inhibiting factor.

Basal plasma prolactin concentration is controlled by tonic inhibition. The major prolactin-inhibiting factor (PIF) is believed to be dopamine. Factors other than dopamine have also been suggested as possible physiological PIF. One of the major candidates for the nondopaminergic PIF is considered to be gamma-aminobutyric acid (GABA). We have carefully examined the possible physiological role of GABA by monitoring, at every 2 min, the circulating prolactin concentration after GABA administration, in conscious freely moving rats. GABA (0.1 or 1 g/kg) had no significant direct effect on plasma prolactin in rats in which the dopaminergic receptors were completely blocked by pimozide, nor in hypophysectomized rats in which a pituitary had been grafted under the kidney capsule and was therefore removed from any hypothalamic influence. The effects of bicuculline, a GABA-receptor-blocking agent, was examined in order to find out whether a tonic inhibition is exerted by GABA after elimination of tonic dopaminergic inhibition on prolactin secretion. The pimozide-treated rat in which the dopaminergic tone is completely eliminated did not show any prominent elevation of plasma prolactin concentration after bicuculline (300 micrograms/kg) administration. However, GABA did have an inhibitory effect in a primary pituitary cell monolayer culture system. Therefore, we conclude that GABA does not play a significant role as a physiological PIF and that the inhibitory effect of GABA in vitro is of a pharmacological nature.

Sustained oestrogen-induced hyperprolactinaemia results from a pituitary defect.

Pituitary enlargement and hyperprolactinaemia were induced in male rats by a single subcutaneous injection of 2 mg oestradiol benzoate in oil. Two months after treatment, when oestrogen levels were normal, serial blood samples for determination of plasma concentrations of prolactin were obtained from undisturbed animals through an indwelling right atrial cannula which had been implanted 7-10 days before. Basal concentrations of prolactin were obtained in treated and control rats, and responses of prolactin to intravenous injections of thyrotrophin releasing hormone (TRH), apomorphine, butaclamol and fenfluramine were measured. Sustained hyperprolactinaemia with pituitary hyperplasia was achieved in only 20% of animals. Responses of prolactin to TRH were the same in control, oestrogen-treated hyperprolactinaemic and non-hyperprolactinaemic rats, indicating normal pituitary responsiveness to one prolactin releasing factor. Complete suppression of prolactin concentrations by apomorphine occurred in hyperprolactinaemic animals, whereas no suppression could be demonstrated in animals with normal (low) basal prolactin levels, indicating good responsiveness of hyperplastic pituitary glands to dopamine inhibition. Dopamine receptor blockade by butaclamol resulted in a vigorous prolactin response in animals with sustained hyperprolactinaemia, indicating that dopaminergic prolactin inhibitory mechanisms remain qualitatively intact, but the response was quantitatively less than in controls, suggesting insufficient hypothalamic release of dopamine. Responses of prolactin to certain doses of fenfluramine were completely abolished in hyperprolactinaemic animals, indicating diminished sensitivity to serotoninergic prolactin releasing factor mechanisms. Prolactin releasing factor unresponsiveness and relative insufficiency of dopaminergic activity could be regarded as physiologically appropriate responses to chronic hyperprolactinaemia. Thus oestrogen-induced chronic hyperprolactinaemia appears to be entirely of pituitary origin.

Twenty-four hour plasma levels of growth hormone and prolactin in Huntington's disease.

Since hypothalamic neural degeneration is thought to occur in individuals with Huntington's disease, anterior pituitary hormone secretion which is in part regulated by the hypothalamus, was postulated to be altered in patients with this disease. To test this proposal, nine females with Huntington's disease were matched with controls to participate in a 24-hour basal level study of growth hormone and prolactin concentration in plasma. Patients who were free from all centrally active medication for at least six months and normal volunteers had blood sampled at 30-minute intervals over 24 hours in a minimal stress environment. The results demonstrated that plasma levels of growth hormone were elevated throughout the 24-hour time period in Huntington's disease individuals. Despite the elevation, the mean growth hormone curve of the Huntington's disease group retained characteristics similar to the control curve throughout the 24-hour time. Basal 24-hour plasma prolactin concentrations in Huntington's disease patients showed no difference from those in control individuals.

Regulation of prolactin secretion in the pregnant pig: effect of fetal hypophysectomy and fetal death in small litters.

Fetal effects on prolactin secretion in late pregnancy and at term were studied in gilts with small litters of intact, hypophysectomized, partially hypophysectomized or dead fetuses. Litter size was reduced at surgery at Days 30-40 of gestation and fetal hypophysectomy or sham procedure attempted on Days 90-95 of gestation using an electrocoagulating probe. Plasma prolactin concentrations rose markedly before parturition in three gilts with normal litters (P = 0.05) and to lower peak concentrations in two gilts with a single fetus. Plasma prolactin did not change from basal concentrations in 4 gilts with small litters (1-2 fetuses) of hypophysectomized fetuses or, in 2 gilts with dead fetuses. Basal plasma prolactin concentrations were significantly lower in gilts carrying hypophysectomized or dead fetuses, compared to normal gilts (P = 0.01). A surge of prolactin secretion preceded delivery in 2 gilts with fetuses with incomplete hypophysectomy and in 1 gilt with 1 of 3 hypophysectomized fetuses. Abnormal patterns of prolactin secretion were seen in 1 gilt with 3 of 5 hypophysectomized fetuses and in 1 gilt with 1 partially hypophysectomized fetus. The results suggest that the fetus may be associated with a mechanism regulating plasma prolactin concentration at term. It is possible that this association may be by way of the fetal pituitary endocrine axes, and/or a function of conceptual mass.

Diminution of prolactin and increase of thyrotrophin response to thyrotrophin releasing hormone occurring independently of changes in basal level of these hormones during treatment of hypothyroidism.

In order to study the effect of rising thyroid hormone levels in hypothyroidism upon prolactin responses to TRH, in relation to changes in basal prolactin concentration and to changes in TSH responses, we followed 18 patients by performing TRH tests before and after 14, 28, 42 and 56 d on gradually increasing levothyroxine dosages, plus a final test when euthyroidism was achieved. Basal prolactin rose initially, at day 14, followed by a return on days 28, 42 and 56 to a level similar to the pretherapeutic value, while at euthyroidism prolactin had fallen below the original value. The area under the prolactin response curve on TRH stimulation was unchanged at 14 d, notwithstanding the rise of basal prolactin concentration. At 28, 42 and 56 d the responses declined progressively along with basal prolactin concentrations that remained equivalent to the pretreatment level. The TSH response to TRH rose at 14, 28, and 42 d along with a continuous downward course of basal TSH. Thus, substitution with L-thyroxine inhibited the responsivity of prolactin but enhanced that of TSH to TRH. The fact that these changes occurred in opposite directions, appears to rule out a negative feed-back effect of T4 on hypothalamic TRH secretion. The effects on responses were shown to occur independently of those on basal secretion of prolactin and TSH.

The Effects of Pyridoxine on Pituitary Hormone Secretion in Amenorrhea-Galactorrhea Syndromes

Pyridoxine (vitamin B6) is metabolized in vivo to pyri-doxal-5′-phosphate, which serves as a cofactor for dopa decarboxylase. This enzyme converts dopa to dopamine, for which reason it has been thought that pyridoxine might function as a dopaminergic agent. The data concerning the effects of pyridoxine on pituitary hormones in normal subjects and in patients with hyperprolactine-mia have been conflicting. The present study was undertaken because of the lack of information concerning the effects of pyridoxine on gonadotropins and because of unexplained reports of the amelioration of galactorrhea by pyridoxine. The study was designed in an attempt to determine if acute or chronic pyridoxine administration could be shown to have any dopamine-like effect on the pituitary function in patients with amenorrhea and galactorrhea. The major emphasis, however, was to evaluate the effect of pyridoxine on prolactin and gonadotropins. Six patients (ages 22 to 37 years) with amenorrhea were studied, five of whom also had galactorrhea and elevated serum prolactin levels. Four provocative or suppressive tests were performed on alternate days after an overnight fast: TRH (500 mg) was injected as an intravenous bolus; L-dopa (500 mg) was given orally; chlorpromazine (25 mg) was injected intramuscularly (four patients); and a 300-mg intravenous bolus of pyridoxine was given. Blood samples were taken at intervals after each test. They were assayed for LH, FSH, and prolactin after L-dopa and chlorpromazine, and for these plus hGH and TSH after pyridoxine and TRH. The patients were then placed on 600 mg of pyridoxine per day orally (in three divided doses) and were readmitted 21 days later for a repeat of the above protocol on pyridoxine. They remained on 600 mg of pyridoxine per day orally for 3 to 4 months, with monthly clinical evaluations and basal serum prolactin, LH, and FSH measurements. The patients were similarly followed for 3 months after discontinuing pyridoxine. There were no significant responses of prolactin, LH, FSH, hGH, or TSH to pyridoxine under either basal or treatment conditions. TRH induced similar responses in plasma TSH before and during administration of pyridoxine. Before therapy, prolactin rose after TRH in four of the six patients. On pyridoxine, prolactin increased after TRH in two patients who had not responded initially. One of these women resumed menses while on pyridoxine. There was, however, no significant difference in mean prolactin reponse to TRH before or during pyridoxine therapy, whether comparison is made of maximum levels or increments of prolactin. The administration of 25 mg of chlorpromazine did not change the basal prolactin, LH, or FSH concentrations in any patient significantly. L-dopa caused a decrease in the basal prolactin concentration in all patients before pyridoxine treatment. The degree of suppression was unchanged after 3 weeks of pyridoxine therapy. Gonad-otropin levels did not change after L-dopa in either the pre- or post-therapy test. The L-dopa-induced rise in GH was unchanged before and after pyridoxine. Within individual tests, both before and after pyridoxine, prolactin increased after TRH and decreased after L-dopa, and hGH increased after L-dopa similarly. The means for each sampling time within tests were, however, significantly different (P < 0.05) for the TSH response to TRH. The mean basal prolactin, LH, and FSH (97.1 ± 14.8 ng/ml, 23.6 mlU/ml, and 18.8 ± 1.9 mlU/ml, respectively) during chronic pyridoxine treatment were not significantly different from pretreatment levels or from those 3 months after cessation of therapy. In addition, the mean basal prolactin of all tests after 21 days of pyridoxine (96.1 ± 10.3 ng/ml) was unchanged. Nevertheless, two of the six patients resumed regular menses during the chronic pyridoxine therapy. These patients had the lowest basal prolactin levels but could not be distinguished from the group on the basis of responses to the provocative tests nor on the basis of hormone levels after chronic therapy. One of these patients continued to have monthly menstrual periods during the 3 months after discontinuing pyridoxine, whereas the other had only two periods with light bleeding. Pretreatment levels of pyridoxal-5′-phosphate and hemolysate pyridoxal kinase were similar among the four patients in whom they were measured. After 3 to 4 months of pyridoxine treatment, the pyridoxal-5′-phosphate concentrations were also similar in the two patients who began menses (3 and 427 ng/1010 red blood cells; 89 and 156 ng/ml of plasma) and two of the patients whose menses did not begin (437 and 153 ng/1010 red blood cells; 126 and 67 ng/ml of plasma). The hemolysate pyridoxal kinase activity was likewise similar in the two pairs. No adverse effects were noted during pyridoxine therapy.

Androgens and prolactin levels in hirsute women with either polycystic ovaries or “borderline ovaries”

The purpose of this study was to investigate the hypothesis that elevated serum prolactin (PRL) levels might explain the adrenal hyperandrogenism which is often associated with the ovarian hyperandrogenism in hirsute women. Accordingly, serum levels of estrone (E 1 ), estradiol (E 2 ), 17-hydroxyprogesterone (17-OHP), testosterone (T), dihydrotestosterone (DHT), androstenedione (∆ 4 A), dehydroepiandrosterone (DHEA), and its sulfate (DHEAS), as well as serum PRL, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and their responses to thyrotropin-releasing hormone (TRH) and LH-releasing hormone (LH-RH) were assayed in 23 hirsute women, 16 with polycystic ovaries (PCO group) and 7 with “borderline ovaries” (BO group: ovaries with a normal appearance at laparoscopy but with histologic abnormalities similar to those of polycystic ovaries). The results were compared with those of 11 normal control subjects. Slightly elevated PRL levels (18 to 32 ng/ml) were found in ten hirsute women. Mean basal concentrations of PRL and LH, mean LH response, and mean concentrations of all the steroids except E 2 were significantly elevated in the PCO group. Most of these elevated hormone levels were present but less pronounced in the BO group. PRL response to TRH was normal in the hirsute women. We found no significant relationship between PRL and steroid hormone values. On the other hand, mean DHEAS, DHEA, and ∆ 4 A concentrations were higher in the group of the ten hirsute women with slightly elevated PRL concentrations than in the group with normal concentrations, but the difference was not significant. Thus, serum PRL is often slightly elevated in hirsute women with ovarian hyperandrogenism, although our data do not clearly support the hypothesis that these elevated concentrations induce the associated adrenal hyperandrogenism.

Effects of dopamine, norepinephrine and serotonin on plasma concentrations of luteinizing hormone and prolactin in ovariectomized and anestrous ewes.

Two experiments were conducted in ovariectomized and anestrous ewes to examine for effects of dopamine (DA), norepinephrine (NE) and serotonin (5-FIT) on basal concentrations of luteinizing hormone (LH) and prolactin (PrI) and the gonadotropin-releasing hormone (GnRH)-induced release of LH. In Experiment 1, ovariectomized ewes, during the breeding and anestrous seasons, were infused for 6 h intravenously with DA (0.66, 6.6 or 66 pg/kg per mm), NE or 5-HT (each at doses of 0.06, 0.66 or 6.6 pg/kg per mm). Effects of the biogenic amines on tonic concentrations and GnRH-induced release of LH were not different between seasons. Prior to GnRH, mean concentrations of LH in plasma were affected by DA, NE and 5-HT in a dose-dependent manner. The high dose of DA and NE decreased mean concentrations of LH, while the high dose of 5-FIT increased mean concentrations of LH during the first 2 h of infusion. Mean concentrations of LH in the 4 h following administration of CnRH were related to mean concentrations of LH prior to GnRH. After adjustment by analysis of covariance, there was a significant effect of the interaction of biogenic amine X dose on mean concentrations of LH following administration of CnRH. Dose-response patterns of LH to administration of GnRFI following infusion of biogenic arnines were similar to those observed prior to treatment with GnRH. While 5-FIT did not affect concentrations of PrI, DA and NE reduced concentrations of PrI. Dopamine was more effective in inhibiting secretion of PrI in fall than in spring. Changes in PrI and LH were not correlated. In Experiment 2, anestrous ewes were infused intravenously with DA (0.66 and 66 pg/kg per mm), NE or 5-HT (each at doses of 0.06 and 6.6 pg/kg per mm). Concentrations of LH were uniformly low prior to administration of CnRH. Following treatment with GnRH, NE inhibited and 5-HT potentiated the release of LH (P<0.01), while DA had no effect. Concentrations of PrI in plasma were inhibited by DA and NE in a dose-related manner (P<0.01). Intravenous infusion of 5-HT did not affect Prl. Again, there was no apparent relationship between changes in LH and PrI.

Effect of supplementary food on suckling patterns and ovarian activity during lactation.

Patterns of infant feeding, basal prolactin concentrations, and ovarian activity were studied longitudinally in 27 breast-feeding mothers from delivery until first ovulation. Suckling frequency (6.1 feeds/day) and suckling duration (122 mins/day) reached peak values four weeks post partum and remained relatively constant until the introduction of supplementary food at a mean of 16 weeks post partum. There were subsequently sharp declines in both the frequency and duration of suckling, both of which correlated closely with basal prolactin concentrations. None of the 27 mothers ovulated during unsupplemented breast-feeding, but within 16 weeks of introducing supplements ovarian follicular development had returned in 20 and ovulation in 14 mothers. The mothers who ovulated within 16 weeks of giving supplements had reduced frequency and duration of suckling more quickly and weaned more abruptly than those who continued to suppress ovulation. These data suggest that the introduction of supplementary food may exert an important and hitherto unrecognised effect on the timing of first ovulation by reducing the frequency and duration of suckling episodes.

Hormonal patterns during heat stress following PGF 2α-tham salt induced luteal regression in heifers

Ten, normally cycling, Holstein heifers were assigned to one of two environmental treatment groups (21.3 C, 59% RH or 32.0 C, 67% RH). PGF 2α was used to induce luteal regression and synchronize estrus in order to evaluate temperature effects on various hormonal and physiological responses during the proestrous through metestrous periods. Environmental temperature (32.0 C) evoked a 1.4 C increase in rectal temperature and a 3.6 C increase in skin temperatures. Length of estrus was shorter (P<.10) for heifers at 32.0 C (16 vs 21 hr.). Average plasma progestin concentration between treatments was not different (P>.10). Mean estradiol concentrations were significantly (P<.10) lower in heifers at 32.0 C. No differences (P>.10) were detected in mean concentrations of LH between heifers at 21.3 C and 32.0 C. Preovulatory peak LH concentrations were 32.2 and 33.2 ng/ml plasma, respectively. All animals had a preovulatory surge of LH, suggesting that hyperthermia did not alter factors which regulate hypothalamic control of LH release. Mean basal concentrations of prolactin and corticoids were not different between temperature treatments (P>.10). However, mean corticoid response following ACTH was of lower magnitude, earlier to peak, and of shorter duration in heat stressed heifers. Heat stress did not appear to affect the hormonal milieu in peripheral plasma associated with corpus luteum regression (decrease in progestin) and ovulation (LH surge). However, duration of estrus, concentrations of estradiol at proestrus and corticoid response to injection of ACTH were reduced.

Testicular function after renal transplantation.

Gonadal function was assessed in seventeen adult male renal transplant recipients, with well established good homograft function, for a mean of 4.9 years. Patients were assessed clinically and by measurement of basal concentrations of FSH, LH, prolactin, testosterone and oestradiol, FSH and LH responses to bolus injections of LHRH and semen analysis. Retrospectively all had symptoms consistent with marked hypogonadism prior to transplantation but in nine out of sixteen this was reversed with transplantation. Residual hypogonadism was evident in seven of sixteen patients and correlated with duration of haemodialysis longer than 1 year (P less than 0.01). Even among patients with clinically normal gonadal function, defects in the hypothalamic--pituitary--testicular axis remained. Elevated basal serum FSH, excessive FSH responses to LHRH and lowered basal serum testosterone were found. In the group with residual hypogonadism more marked changes, including elevated basal LH and excessive LH responses to LHRH, were also found. Fertility was recorded in two men on three occasions since transplantation. Sperm counts were normal in five and abnormal in four patients. Testicular volume and sperm density were inversely correlated with basal and stimulated FSH and LH levels.

Short- and long-term fluctuations in plasma prolactin concentration in normal subjects.

The physiological changes in plasma prolactin concentration were studied in 447 normal subjects, including 65 men, 75 pre-menopausal women and 307 post-menopausal women. The within-day and day-to-day variation as well as the circadian and circannual rhythm of plasma prolactin levels were determined. Furthermore, the relationship between changes in prolactin and oestradiol-17 beta levels during the normal menstrual cycle and in the climacteric was studied. Pre-menopausal women had significantly (P less than 0.01) higher basal plasma prolactin concentration than men and post-menopausal women. Furthermore, they had significantly (P less than 0.01) higher day-to-day variation than men. This suggests that prolactin in women is secreted in a pulsatile fashion. Only small seasonal variations in both sexes were seen. The levels of plasma prolactin during the ovulatory and the luteal phase in the cycle were significantly (P less than 0.02) higher than that of the follicular phase, and a positive correlation between changes in plasma concentration of oestradiol-17 beta and prolactin was found. Also in post-menopausal women a relationship between plasma concentration of prolactin and oestradiol-17 beta was seen. It is concluded that the assessment on the physiological variation recorded during sleep in both sexes. However, only in women day-to-day changes and the changes related to the menstrual cycle and the climacteric are of importance.

Prolactin pulsatility in patients with gonadal dysfunction.

Serum prolactin concentrations have been measured at 15 min intervals for 2 h on 240 occasions in 227 patients with symptoms which could have been due to hyperprolactinaemic gonadal dysfunction. Of the 227, 138 had at least one elevated random prolactin level. Overall, 22% showed no significant fluctuation in prolactin. In 38% the levels fell progressively from the start of the sampling period, this pattern being found most commonly in patients complaining of infertility. The sampling method yielded a basal or unstressed prolactin concentration which was, on average, 27% lower than random prolactin concentrations. However, a comparison with clinical data, the radiological appearances of the pituitary fossa, and the response to bromocriptine therapy, has shown that there is no predictive information in the multiple sampling results that could not have been obtained from two or three random prolactin levels.

Effect of sleep deprivation on dopamine receptor function in normal subjects.

Twenty-four hours sleep deprivation significantly decreased the growth hormone response to the dopamine receptor agonist, apomorphine HCl, in five normal men (0.5 mg s.c.) and one woman (0.75 mg s.c.) but had no effect on basal or post-apomorphine prolactin concentrations. These results suggest that sleep deprivation decreases the sensitivity of certain central dopamine receptors. The relevance of this finding to the antidepressant effect of sleep deprivation is unclear.

Periparturient and Postpartum Endocrine Changes of Conceptus and Maternal Units in Jersey Cows Bred for Milk Yield

Control cows, sired and bred by bulls of zero estimated breeding value, and selected cows, sired by and bred to bulls of high predicted differences for milk yield, were used to evaluate maternal endocrine changes from 14 days prepartum to 28 days postpartum. Examined were concentrations in plasma of 13, 14 dihydro-15 keto-prostaglandin F2α, progesterone, estrone sulfate, estrone, luteinizing hormone, and prolactin. Ability of cows to release prolactin and luteinizing hormone on day 10 postpartum was evaluated after a simultaneous injection of thyrotropin releasing hormone (100μg) and gonadtropin releasing hormone (100μg). Changes in progesterone and estrogens prepartum lead to peak concentrations of prolactin and prostaglandin at parturition and 3 days postpartum, respectively. Higher basal concentrations of prolactin for control cows prepartum were associated with a higher prolactin release by thyrotropin releasing hormone at 10 days postpartum. Although release of luteinizing hormone in response to gonadotropin releasing hormone did not differ between groups on day 10 postpartum, a subsequent increase in progesterone to above 1ng/ml was earlier and more precisely synchronized among control cows (16±.43 versus 23±2.33 days). Within cow concentrations of F2α13, 14 dihydro-15-keto-prostaglandin-F2α were correlated with size of previous gravid uterine horn (.67) and milk yield (−.39). Selection for milk yield influenced postpartum endocrine function.

Effect of TRH on the secretion of prolactin in ewes at various stages of pregnancy and in non-pregnant ewes during the breeding season and seasonal anoestrus.

The concentrations of prolactin in plasma were measured before and after the injection of TRH in pregnant ewes and in non-pregnant ewes during the breeding season and seasonal anoestrus. During the first 80 days of pregnancy basal concentrations or prolactin were low and stable but thereafter increased progressively to reach maximum values at Day 140. During a comparable time of year (December-April) basal concentrations of prolactin in non-pregnant ewes were not significantly different from those found between Days 20 and 120 of pregnancy. At other times of the year basal concentrations of prolactin in non-pregnant ewes were elevated during anoestrus and declined markedly at the onset of the breeding season. In pregnant and non-pregnant ewes the responsiveness of the pituitary gland to stimulation with TRH was significantly correlated with the basal concentration of prolactin in plasma: the raised concentration of prolactin at Day 140 of pregnancy and in July in non-pregnant ewes was associated with the greatest release of prolactin from the pituitary gland. A change in the responsiveness of the pituitary gland may play an important role in the overall control of prolactin secretion in the ewe.

Spontaneous and melatonin-induced testicular regression in male golden hamsters: augmented sensitivity of the old male to melatonin inhibition.

Effects of aging and melatonin on testicular function of golden male hamsters were investigated. Young (3-4 months) and old (22-26 months) male hamsters were maintained on a long photoperiod (14 h light, 10 h dark) and injected with graded doses of 10, 25, 50 microgram melatonin or injection vehicle, at 17:00 h (3 h before lights off) for a period of 6 weeks. Old male hamsters had significantly decreased testicular weights as compared with the young counterparts, but accessory sex organ (seminal vesicles and accessory glands) weights did not differ between young and old male hamsters. All doses of melatonin suppressed testicular and accessory sex organ weights in the young as well as in the old animals. The percent decrease in testicular weight in response to melatonin treatment was significantly greater (p less than 0.01) in the old than in the young hamsters. Basal plasma prolactin concentration did not differ between young and old male hamsters. Melatonin significantly decreased plasma prolactin concentrations in both age-groups. Young hamsters had greater mean plasma luteinizing hormone concentrations than old hamsters, and melatonin suppressed luteinizing hormone equally in both groups. These results indicate that the testes of the male hamster spontaneously regress during the aging process, and this may be independent of prolactin, since there was no difference in serum prolactin concentrations between young and old hamsters. The finding that melatonin injections brought about a greater percent decrease in testicular weight in the old than in the young hamsters suggests that there is an increased sensitivity of the reproductive system to melatonin inhibition in the old male hamster.