Luteinizing hormone-releasing factor potentiates lordosis behavior in hypophysectomized ovariectomized female rats

Subcutaneous injection of luteinizing hormone-releasing factor (LRF) in estrogen-primed hypophysectomized, ovariectomized female rats facilitates the appearance of the lordosis response. The LRF effect on lordosis was seen 90, 180, and 360 minutes after injection. This effect could help to synchronize the female's mating behavior with the ovulatory discharge of luteinizing hormone.     

Gamma-aminobutyric acid effects on pituitary gonadotropin secretion

Gamma-aminobutyric acid (GABA) injected into the third ventricle of male rats promotes the release of pituitary luteinizing hormone (LH) but not follicle-stimulating hormone. When GABA was injected directly into the pituitary it was ineffective in promoting LH release. This evidence suggests that GABA may play a role in controlling the discharge of hypothalamic luteinizing hormone releasing factor.     

Luteinizing hormone-releasing activity in hypophysial stalk blood and elevation by dopamine

Pituitary halves incubated in pituitary stalk plasma release more luteinizing hormone than their opposite halves incubated in plasma from peripheral blood. Glands incubated in stalk plasma from dopamine-treated rats release more luteinizing hormone than glands incubated in stalk plasma from untreated controls. Luteinizing hormone-releasing activity in stalk plasma may be due to the luteinizing hormone-releasing factor, and the secretion of luteinizing hormone-releasing factor may be controlled by a dopaminergic mechanism.     

Progesterone administration in vivo stimulates release of luteinizing hormone-releasing hormone in vitro

The release of luteinizing hormone-releasing hormone (LHRH) from tissue from the mediobasal hypothalamic-anterior hypothalamic-preoptic area of prepuberal female rats was measured in a perfusion system. Measurements were also made of the concentrations of LHRH in these tissue fragments and of luteinizing hormone in serum obtained when the rats were killed. Four groups of immature rats were studied: intact, ovariectomized, ovariectomized and implanted with estradiol-containing capsules, and ovariectomized rats primed with estradiol and injected with progesterone. The release of LHRH from the tissue of ovariectomized animals was significantly less than that of intact females and was not modified when the ovariectomized rats received estradiol. However, there was a four- to fivefold increase in LHRH release from tissue of ovariectomized rats primed with estradiol when they were killed 6 hours after they received an injection of progesterone. The concentrations of LHRH in tissue and of luteinizing hormone in serum varied among groups and with the time of day that the animals were killed. The interactions among luteinizing hormone, gonadal steroids, and the photoperiod seem to set the appropriate conditions for neural processes triggering a complete and normal release of luteinizing hormone.     

Inhibin-mediated feedback control of follicle-stimulating hormone secretion in the female rat

The secretion of follicle-stimulating hormone (FSH) by the anterior pituitary gland is regulated by the interaction of hypothalamic and gonadal hormones. Recently, proteins termed inhibins that selectively suppress FSH secretion have been purified and characterized from the gonadal fluids of several species. Antibodies to a synthetic peptide encompassing the amino terminal 25 residues of the recently characterized porcine inhibin were used to develop a specific radioimmunoassay (RIA) for inhibin and to neutralize endogenous inhibin during the estrous cycle of the rat. The administration of 20 international units of pregnant mare serum gonadotropin (PMSG) stimulated the secretion of inhibin in intact immature female rats, whereas ovariectomy caused an abrupt decrease in plasma inhibin concentrations that were not prevented by the injection of PMSG. The infusion of a polyclonal antiserum to inhibin, from 12 noon on proestrus to 1 a.m. on the morning of estrus, as well as its acute intravenous injection during diestrus I or II, caused an increase in plasma FSH (but not luteinizing hormone) concentrations. These results support the hypothesis of a feedback loop between the release of ovarian inhibin and FSH in the female rat.     

Prostaglandin involvement in hypothalamic control of gonadotropin and prolactin release

Prostaglandin E(2) (PGE(2)) injected into the third ventricle of ovariectomized rats increased plasma luteinizing hormone dramatically and follicle stimulating hormone slightly. PGE(1) elevated prolactin; PGF(1alpha) or PGF(2alpha) had no effect. PGE(2) or PGE(1) injected directly into the anterior pituitary were ineffective. These results suggest that specific prostaglandins act at the hypothalamus to control pituitary hormone release.     

Induction of ovulation in immature hypophysectomized rats

Immature rats given minute doses of highly purified pituitary gonadotropins (follicle-stimulating hormone and luteinizing hormone) 7 to 100 days after hypophysectomy ovulated and formed corpora lutea. Neither hormone alone was effective. Luteinizing hormone repaired in part the atrophied theca interna and interstitial tissue, and follicle-stimulating hormone stimulated the development of the granulosa cells.     

Brain receptors sensitive to indole compounds: function in control of luteinizing hormone secretion

The placement of melatonin and of 5-hydroxytryptophol in the median eminence of castrated male rats is followed 5 days later by a significant decrease in pituitary stores of luteinizing hormone. Pituitary reserve of this hormone is also depleted after the implantation of melatonin, 5-hydroxytryptophol, and 5-methoxytryptophol in the reticular formation of the midbrain. It is suggested that these indole compounds, which are normally synthesized in the pineal gland, may intervene in the control of the secretion of luteinizing hormone, possibly by acting on specific receptors localized in the median eminence and in the midbrain.     

Prolactin stimulation of maternal behavior in female rats

Inexperienced, hypophysectomized female rats treated with steroids were used in experiments to investigate the roles of the pituitary gland and prolactin in the expression of maternal behavior. Administration of ovine prolactin or treatment with ectopic pituitary grafts, which release prolactin into the circulation, stimulated maternal care in these females toward rat young. Steroid treatment alone, while stimulating maternal behavior in rats with intact pituitary glands, did not facilitate maternal responsiveness in hypophysectomized females. These findings indicate a stimulatory behavioral role for pituitary prolactin in the establishment of maternal care and suggest that exposure to prolactin during pregnancy helps to stimulate the immediate onset of maternal behavior at parturition.     

Hypophyseal control of genetic expression during chick feather and skin differentiation

The normal sequence of molecular events which occurs during feather and skin differentiation in the chick embryo is interrupted by pituitary gland ablation. The characteristic pattern of development is reestablished in hypophysectomized embryos treated with pituitary extract and in hypophysectomized embryos in parabiotic union with their twins within a double-yolked egg. These results suggest that genetic expression in differentiating chick feather and skin after day 12 of incubation is regulated by hormones.     

Dopamine synthesis: stimulation by a hypothalamic factor

The effect of treatment with the factor that inhibits the release of melanocyte stimulating hormone (MSH) identified as 1-prolyl-1-leucylglycinamide (MIF) on brain catecholamine synthesis was examined in normal and hypophysectomized rats. The tripeptide induced a dose-related increase in striatal dopamine synthesis in slices obtained from treated normal animals but not in hypophysectomized animals. Hypothalamic norepinephrine synthesis was unaltered by MIF treatment in normal as well as in hypophysectomized rats. In addition, dopamine and norepinephrine syntheses were depressed in untreated hypophysectomized animals, as compared to normal controls. These results constitute the first direct demonstration of a central neurochemical effect of a hypothalamic factor.     

Pituitary-adrenal influences on fear responding

In a passive avoidance situation, hypophysectomized male rats show less fear than normal rats, whereas adrenalectomized rats show greater fear than normals. These results probably occur because hypophysectomized rats lack adrenocorticotrophic hormone, which increases arousal or emotionality, whereas adrenalectomized animals lack certain adrenal steroids, which inhibit excitatory effects. The results indicate that adrenocorticotrophic hormone and certain adrenal steroids have opposite effects in regulating fear-motivated behavior.     

Thyrotropin releasing hormone: enhancement of dopa activity by a hypothalamic hormone

Thyrotropin releasing hormone potentiates the behaviorial effects of dopa plus pargyline in mice. Because the potentiation occurs in hypophysectomized mice, as well as in normal mice, the phenomenon is independent of the release of thyroid stimulating hormone from the pituitary. Possible mechanisms and clinical implications are discussed.     

Multiple circadian oscillators regulate the timing of behavioral and endocrine rhythms in female golden hamsters

A single daily "surge" in pituitary luteinizing hormone release was observed in ovariectomized-estrogen-treated hamsters expressing an intact circadian rhythm of locomotor activity. In contrast, two luteinizing hormone surges occurred within a single 24-hour period in hamsters whose activity rhythm had dissociated or "split" into two distinct components. These observations indicate that both behavioral and endocrine circadian rhythms are regulated by the same multioscillator system, which seems to be composed of at least two distinct circadian oscillators.     

Daily variation in concentration of cortisol in plasma in intact and hypophysectomized gulf killifish

A daily variation in concentration of cortisol in plasma is synchronized by a 12-hour daily photoperiod in intact as well as in hypophysectomized fish. The daily rhythm in concentration of the adrenal steroid does not depend on a daily rhythm in the concentration of pituitary adrenocorticotropic hormone.     

Synthetic polypeptide antagonists of the hypothalamic luteinizing hormone releasing factor

Two analogs of the hypothalamic luteinizing hormone releasing factor modified at the histidine-2 position were tested for biological activity (secretion of luteinizing hormone) in cultures of dispersed rat anterior pituitary cells. The analog in which glycine was substituted for histidine at position 2, [Gly(2)]LRF, behaves as a partial agonist releasing less than 50 percent of the luteinizing hormone secreted at maximum concentrations of the releasing factor, while the analog in which histidine at position 2 is deleted has no significant agonist activity at any of the doses tested. When added to the cultured cells at molar ratios 10(3) to 10(4) times that of the luteinizing hormone releasing factor, both analogs decrease the amount of luteinizing hormone secreted in response to the releasing factor.     

冷适应对大鼠仔鼠和雏鸡某些内分泌腺和激素水平的影响

以20只健康Wistar大鼠仔鼠和30只罗曼雏鸡为试验对象，研究冷适应对大鼠仔鼠和雏鸡某些内分泌腺和激素水平的影响。冷适应组大鼠肾上腺皮质束状带宽度和肾上腺皮质束状带的细胞数目极显著和显著（P＜0、05）地高于常温对照组，60日龄仔鼠在冷暴露72小时后，冷适应组T3和皮质醇明显升高，T3比常温组提高19．％，皮质醇比常温组提高37．17％而GH、T4及Ins变化不明显。冷适应组雏鸡肾上腺肾间组织面积和肾间组织细胞数分别比常温组提高26．05％和3．25％，垂体嗜酸性细胞和嗜碱性细胞数目分别比常温组提高12．98％和8．59％。雏鸡在35日龄试验结束时，冷适应组T3，T4和胰岛素分别较常温组抵63．85％、44．22％31．85（P＜0．05），而皮质醇比常温组提高90．37％。     

Suppression of ovulation in the rat by an orally active antagonist of luteinizing hormone-releasing hormone

A synthetic antagonist of luteinizing hormone-releasing hormone blocked ovulation in rats in a dose-dependent manner when given by gavage on the afternoon of proestrus. Ovulation was delayed for at least 1 day in all animals given 2 milligrams of antogonist and in some of the animals treated with 1 or 0.5 milligram. Oral administration of 2 milligrams also blocked the preovulatory surge of luteinizing hormone. This demonstration that antagonists of luteinizing hormone-releasing hormone can have oral antiovulatory activity clearly enhances their therapeutic potential.     

Paradoxical elevation of growth hormone by intraventricular somatostatin: possible ultrashort-loop feedback

Somatostatin, the growth hormone-inhibiting factor, when microinjected into the third ventricle of the rat brain, paradoxically induced the release of growth hormone. A pituitary site of action having been ruled out, this result supports the concept that exogenous somatostatin within the hypothalamus acts either to suppress the release of somatostatin from somatostatin-containing neurons, possibly via an ultrashort-loop feedback mechanism, or to augment release of hypothalamic growth hormone-releasing factor, thereby inducing a release of growth hormone. Injection of somatostatin into the third ventricle also decreased plasma concentrations of luteinizing hormone, follicle-stimulating hormone, and thyroid-stimulating hormone, probably by inhibiting the release of luteinizing hormone-releasing factor and thyrotropin-releasing factor.     

Ornithine decarboxylase stimulation in rat ovary by luteinizing hormone

In normal albino rats with a 4-day estrous cycle, the activity of ovarian ornithine decarboxylase undergoes a transitory rise on the evening of proestrus and only at that time. The response could be elicited by the administration of either luteinizing hormone or human chorionic gonadotrophin. When antiserum to luteinizing hormone was injected at 2 p.m. on the day of proestrus, the induction of ornithine decarboxylase was blocked, an indication that the enzyme is under luteinizing hormone control. The strategic positioning of the induction of ornithine decarboxylase between the normal release of luteinizing hormone and ovulation impties that putrescine is associated with the ovulatory process, and opens a new avenue of research on the control of ovulation.