Effects of serotonergic agents on plasma prolactin levels in pyridoxine-deficient adult male rats

Plasma concentration of prolactin was significantly reduced in pyridoxine-deficient as compared to control (pyridoxine-supplemented) adult male rats. Administration of pyridoxine to deficient rats resulted in a significant increase in plasma prolactin. The reduction in plasma prolactin in pyridoxine-deficient rats corresponded with the significantly reduced hypothalamic contents of pyridoxal phosphate and serotonin in pyridoxine-deficient rats. Plasma prolactin concentrations were also measured in response to serotonergic agents in both groups of rats. The administration of the 5HT_1A agonist (8-hydroxy 2-n-dipropylamino tetralin) resulted in a significant increase in plasma prolactin and that of the specific 5HT_1A antagonist spiroxatrine had the opposite effect. The results suggest that the hypothalamic serotonergic regulation of prolactin release is impaired in pyridoxine deficiency.     

Effects of arginine vasotocin on levels of plasma gonadotropins and prolactin in ovariectomized conscious rats

Arginine vasotocin was injected into the third ventricle or intravenously in conscious, ovariectomized rats and its effect on gonadotropin and prolactin release evaluated. The peptide lowered plasma levels of both LH and prolactin in doses of 40 or 100 ng given intraventricularly. The higher dose was slightly more effective than the lower dose. Intravenous injection of a 1-microgram dose of vasotocin failed to alter plasma LH in the ovariectomized animals; however, a 5-micrograms dose induced a slight depression apparent at only 60 min following injection. Intravenous injection of 1 microgram produced a significant lowering of plasma prolactin, whereas a dramatic lowering followed the injection of the higher dose. Plasma FSH was unaffected in these experiments. Incubation of dispersed anterior pituitary cells from ovariectomized rats with various doses of vasotocin revealed no effect of the peptide on the release of FSH, LH, or prolactin. It also did not alter the response to LHRH, but it partially blocked the action of dopamine to inhibit prolactin release. The data indicate that quite low doses of arginine vasotocin act within the brain to inhibit LH and prolactin secretion in ovariectomized, conscious animals.     

Peripheral plasma prolactin and progesterone levels in pseudopregnant goats during bromocryptine treatment

Persistence of luteal function and accumulation of fluid within the uterus (hydrometra) are characteristics of pseudopregnancy in goats. To study the luteotrophic role of prolactin in this condition, seven seudopregnant goats were treated with bromocryptine (1 mg subcutaneously, twice daily) for 6 to 10 d. Plasma progesterone (P4) and prolactin (PRL) were measured by radioimmunoassay (RIA) in samples taken twice daily by venipuncture. Ultrasound scanning took place at regular intervals to visualize the presence of fluid within the uterus. Bromocryptine treatment effectively reduced the plasma PRL concentration in six goats. In all seven goats, a gradual decrease of the plasma P4 concentration to levels < 1.8 ng/ml occured during treatment. After bromocryptine treatment, P4 concentrations reached basal levels (<0.1 ng/ml) in two animals. In four goats, P4 concentrations remained close to 1.0 ng/ml, or even temporarily rose above the 2.0 ng/ml level. Spontaneous discharge of uterine fluid took place during (two goats) or within 4 d after bromocryptine treatment (three goats). These results indicate that prolactin plays an important luteotrophic role during pseudopregnancy in goats.     

Effects of thermal stress on plasma concentrations of luteinizing hormone, progesterone, prolactin and testosterone in the cycling ewe

Naturally cycling white faced ewes were utilized to study the effects of continuously elevated environmental temperature and/or humidity on plasma concentrations of luteinizing hormone (LH), prolactin (PRL), progesterone (P4) and testosterone (TE) during the estrous cycle. Fourteen ewes were randomly allocated on the day of estrus (day 0) to either thermoneutral conditions (21.1 degrees C, 65% relative humidity) or elevated ambient temperature/humidity conditions (36.1 degrees C, 71% relative humidity) producing an average 1.4 degrees C hyperthermia. Animals remained in their respective environments and blood samples were collected daily until the next estrus or day 20, whichever occurred first. Starting at noon on day 14, blood was sampled every 2 hours. Concentrations of LH, PRL, P4 and TE were quantified using validated radioimmunoassays. Hyperthermic ewes exhibited 1) a significant decrease (P<0.05) in the incidence of behavioral estrus and a preovulatory LH surge at the expected time of the estrous cycle, 2) significantly lower (P<0.05) plasma P4 between days 7 and 13 of the cycle, 3) a six-fold increase of PRL levels (P<0.01). Plasma levels of TE were not significantly affected by hyperthermia. The only two experimental ewes which exhibited estrus and an LH surge also showed an unusual and significant peak in plasma P4 two days before estrus. These results confirm that elevated environmental temperatures that result in hyperthermia can induce endocrine imbalances in the ewe which may contribute to decreased reproductive efficiency in the heat-stressed female.     

Effects of morphine and naloxone on serum LH, FSH and prolactin levels and on hypothalamic content of LH-RF in proestrous rats.

Proestrus surges of serum LH, FSH and prolactin (PRL) were significantly reduced when morphine HCl (50 and 10 mg/kg) was administered to 4-day cycling rats just prior to the proestrous critical period. The inhibitory effect of morphine was reversed by naloxone, a morphine antagonist, at the dose which had no effect on the proestrus surges of serum LH, FSH or PRL. The hypothalamic LH-RF content of proestrous rats at 1800 hr (during the proestrus surge) was not significantly different from that at 1400 hr (before the surge) and was not affected by pretreatment with morphine or naloxone. Our results suggest that naloxone reverses the anti-ovulatory effect of morphine by antagonizing the inhibitory effect of morphine on preovulatory surges of gonadotropins or PRL.     

Effects of pargyline on hypothalamic biogenic amines and serum prolactin. LH and TSH in male rats.

The time course effects of pargyline on hypothalamic biogenic amines and serum prolactin (PRL), LH and TSH were studied in adult male rats. The rats were killed at intervals of 1–6 hrs after pargyline injection. Hypothalamic dopamine (DA) rose 79% by 1 hr and was 41% above “0” time by 6 hrs. Norepinephrine (NE) increased 31% by 1 hr and remained at about this level through 6 hrs, whereas serotonin (5HT) increased from 42% by 1 hr and to 95% by 6 hrs. Serum PRL LH and TSH fell significantly during the first 2 hrs, but all had returned to pretreatment values by 4 hrs. Serum PRL was about 4-fold above pretreatment values by 6 hrs, but LH and TSH remained at pretreatment levels. Stimulation by pargyline of PRL release was potentiated by Lilly compound 110140, a serotonin reuptake inhibitor, and blocked by parachlorophenylalanine, a serotonin synthesis inhibitor. These results suggest that the inhibitory effects of pargyline on PRL, LH, and TSH release during the first 2 hrs were associated mainly with a rapid increase in DA, and subsequent elevation of PRL release was related to the increase in 5HT. Return of serum LH and TSH to pretreatment levels at 4 and 6 hrs appeared to be associated mainly with the decrease in DA and perhaps to elevated NE levels. These results suggest that changes in relative concentrations of hypothalamic amines are related to differential release of PRL, LH and TSH.     

Carbidopa elevates hypothalamic dopa and serum prolactin in rats.

The administration of carbidopa (MK-486, α-methyl-L-dopa hydrazine; 100–200 mg/kg, intraperitoneally) causes several-fold increases in hypothalamic dopa and serum prolactin levels in male rats within 2 hours; these changes are not reversed by the administration of pyridoxine. These observations suggest that high doses of carbidopa can affect catecholamine synthesis within the hypothalamus.     

Effects of melatonin and natural and synthetic analogues of arginine vasotocin on plasma prolactin levels in adult male rats

A significant elevation in plasma prolactin was observed 10 min following the intravenous injection of 100 microgram of melatonin into either estrogen-progesterone (EP) primed or into nonsteroid-treated male rats. 60 min postinjection in the EP primed rat, the groups treated with 100 microgram or 10 mg of melatonin had signficantly elevated plasma prolactin levels while no effect was observed with these same doses in the nonsteroid-treated rats. Compared to diluent-treated controls, a significant elevation in plasma prolactin was observed at 10, 20 and 60 min following the intravenous injection of either 1 microgram arginine vasotocin (AVT) or 1 mg melatonin into EP primed male rats. A consistent rise in plasma prolactin was also evident after the injection of 1 microgram of either arginine vasopressin, lysine vasopressin or AVT. Oxytocin had no effect on plasma prolactin values. The intravenous administration of 1 microgram of (deamino-1,6 dicarba, 8-arginine)-vasotocin caused a significant elevation of plasma prolactin 10 and 20 min after injection. However, the injection of another analogue of AVT, (4-leucine, 8-arginine)-vasotocin, had no effect on prolactin release at the time points measured.     

Effects of bromocriptine and perphenazine on prolactin and progesterone concentrations in pregnant pony mares during late gestation

Pregnant pony mares in Group A (n = 4) received i.m. injections at 07:00 and 17:00 h of 0.8 mg bromocriptine/kg body weight 0.75 per day beginning on Day 295 of gestation and continuing until parturition. Group B (n = 4) was treated similarly, but perphenazine was administered orally at 0.375 mg/kg body weight twice a day beginning on Day 305 of gestation and continuing until parturition. Mares in Group C (n = 3) received i.m. injections of saline. Mean plasma prolactin and progesterone concentrations were greater (P less than 0.05) for mares in Group C than in Groups A and B from 295 to 309 days of gestation. From 305 days of gestation, plasma prolactin and progesterone concentrations were greater (P less than 0.05) in Group B and C than in Group A mares. Progesterone and prolactin concentrations increased over this period for Group B and Group C mares, but remained constant in Group A mares. From 10 days pre partum through foaling, mares in Group A had lower progesterone (P less than 0.05) and prolactin (P less than 0.01) concentrations than Group B and C mares. All mares in Group A were agalactic at foaling, while all mares in Groups B and C had normal milk secretion. Gestation was longer (P less than 0.05) in Group A than in Group C mares. In Group A, 2 mares retained the placenta for greater than 3 h, 3 mares had dystocia and all 4 mares had thickened, haemorrhagic placentae.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of a long-acting LHRH agonist preparation on plasma gonadotropin and prolactin levels in castrated male rats and on the release of prolactin from ectopic pituitaries

We have examined the effects of a single subcutaneous injection of an LHRH agonist, D-Trp-6-LHRH, in biodegradable microcapsules of poly(DL-lactide-co-glycolide) on plasma gonadotropin and prolactin (PRL) levels in castrated and in castrated-hypophysectomized-pituitary grafted (CAST-APX-GRAFT) male rats. The results were compared to the effects of daily injections of the same LHRH agonist dissolved in saline. In castrated rats, there were no significant alterations in plasma LH or PRL levels during the 10 days following the injection of LHRH agonist microcapsules, while FSH levels were generally reduced. In castrated males given daily injections of 6 micrograms of LHRH agonist in saline, plasma LH levels were significantly reduced while plasma PRL levels were not changed. In CAST-APX-GRAFT rats, both D-Trp-6-LHRH microcapsules and daily LHRH agonist injections appeared to increase plasma PRL levels. The pattern of changes in PRL release in both groups was similar, with levels on day 6 being significantly higher than those measured on days 1, 3 and 10 after onset of treatment. As expected, LH and FSH levels in these animals were extremely low. Immunoreactive D-Trp-6-LHRH was consistently detectable in the plasma of CAST-APX-GRAFT animals after microcapsule administration, whereas in animals given daily injections of this agonist in saline, its plasma concentrations were often below the detectability limit of the employed assay. These findings suggest that the LHRH agonist, D-Trp-6-LHRH, is capable of causing a short term stimulation of PRL release from ectopic pituitaries. Elevation of plasma LH levels is apparently not required for this effect.     

Effects of progesterone on prolactin secretion in hypogonadal women

Although estrogen is known to stimulate the secretion of prolactin, there are only slight differences between the prolactin levels in the follicular and luteal phases in normal women. To test the hypothesis that progesterone is involved in the regulation of prolactin release, 50 mg of progesterone was administered intramuscularly at 0600 h to twelve hypogonadal women and blood samples were obtained at 15 min intervals between 1500 and 2000 h to determine the prolactin levels. The day before progesterone treatment, control blood samples were obtained at 15 min intervals between 1500 and 2000 h. The serum progesterone levels were 28.7 +/- 4.1 ng/ml at 1500 h, 24.2 +/- 3.5 ng/ml at 1730 h and 21.3 +/- 2.9 ng/ml (mean +/- SD) at 2000 h. In eight of twelve hypogonadal women, progesterone lowered circulating prolactin levels significantly. These results indicate that a high level of progesterone in the luteal phase may partly block estrogen-induced prolactin release physiologically.     

Effects of hypothalamic lesions on levels of plasma free fatty acids in the mallard duck.

Plasma free fatty acid (FFA) levels were measured in the mallard duck (Anas platyrhynchos) following hypothalamic lesions at various sites. The results indicate that ventromedial lesions produced hyperphagia, increased deposition of fat, and significantly elevated levels of plasma FFA. Anterior bilateral lesions resulted in aphagia, severe loss in body weight and a marked decrease in plasma FFA. Lesions in other regions of the hypothalamus produced various changes depending upon the extent of damage. The neural and neuroendocrine mechanisms which regulate FFA levels in the blood are discussed with respect to the involvement of pituitary hormones.     

Effect of induced suprabasal progesterone levels around estrus on plasma concentrations of progesterone, estradiol-17beta and LH in heifers

A controlled study was carried out to investigate the effects of suprabasal plasma progesterone concentrations on blood plasma patterns of progesterone, LH and estradiol-17beta around estrus. Heifers were assigned to receive subcutaneous silicone implants containing 2.5 g (n=4), 5 g (n=4), 6 g (n=3), 7.5 g (n=3) or 10 g (n=4) of progesterone, or implants without hormone (controls, n=5). The implants were inserted on Day 8 of the cycle (Day 0=ovulation) and left in place for 17 d. The time of ovulation was determined by ultrasound scanning. Blood was collected daily from Days 0 to 14 and at 2 to 4-h intervals from Days 15 to 27. Control heifers had the lowest progesterone concentrations on Days 20.5 to 21 (0.5 +/- 0.1 nmol L(-1)); a similar pattern was observed in heifers treated with 2.5 and 5 g of progesterone. In the same period, mean progesterone concentrations in the heifers treated with 6, 7.5 and 10 g were larger (P < 0.05) than in the controls, remaining between 1 and 2.4 nmol L(-1) until implant removal. A preovulatory estradiol increase started on Days 16.4 to 18.4 in all the animals. In the controls and in heifers treated with 2.5 and 5 g of progesterone, estradiol peaked and was followed by the onset of an LH surge. In the remaining treatments, estradiol release was prolonged and increased (P < 0.05), while the LH peak was delayed (P < 0.05) until the end of the increase in estradiol concentration. The estrous cycle was consequently extended (P < 0.05). In all heifers, onset of the LH surge occurred when progesterone reached 0.4 to 1.2 nmol L(-1). The induction of suprabasal levels of progesterone after spontaneous luteolysis caused endocrine asynchronies similar to those observed in cases of repeat breeding. It is suggested that suprabasal concentrations of progesterone around estrus may be a cause of disturbances oestrus/ovulation.