The effect of LH-RH administration on LH release in the female rabbit.

Intracarotid infusion of LH-RH to female rabbits stimulated a significant increase in plasma LH concentration in the jugular vein. This response varied with the reproductive state of the animal, with a greater release occurring in oestrous (spontaneous or oestrogen-induced) and non-receptive does than in pseudopregnant or ovariectomized animals. If ovariectomized rabbits were pretreated with oestrogen, the pituitary response to LH-RH was restored. These findings suggest that there is little change in pituitary sensitivity to LH-RH infusion between oestrous and non-receptive rabbits, although pseudopregnancy (high physiological levels of progesterone) or ovariectomy inhibit its ability to respond to a releasing-hormone stimulus.     

Effect of mating stimuli on LH release in bulls

Fourteen crossbred beef bulls were assigned at random to receive one of four sexual stimuli treatments. Treatments consisted of: (1) controls (four bulls), no visual or physical contact with any cows; (2) false mount (two bulls), allowed to mount an estrual cow; (3) mated (four bulls), allowed to mount an estrual cow with intromission and ejaculation; (4) electroejaculated (four bulls), no exposure to cows. Serum from blood samples taken at 15-min intervals from -15 min to 2 hr from sexual stimuli were radioimmunoassayed for luteinizing hormone (LH). Four bulls had elevated levels at the pretreatment bleeding, but none of the stimuli induced or were associated with LH releases. Basal levels of LH were consistent within bulls but varied considerably among bulls. Conclusion is that stimuli associated with mating do not cause a release of LH.     

Estrogen and leptin have differential effects on FSH and LH release in female rats

Prior experiments have shown that the adipocyte hormone leptin can advance puberty in mice. We hypothesized that it would also stimulate gonadotrophin secretion in adults. Since the secretion of follicle stimulating hormone (FSH) and luteinizing hormone (LH) is drastically affected by estrogen, we hypothesized that leptin might have different actions dependent on the dose of estrogen. Consequently in these experiments, we tested the effect of injection of leptin into the third cerebral ventricle of ovariectomized animals injected with either the oil diluent, 10 microg or 50 microg of estradiol benzoate 72 hr prior to the experiment. The animals were ovariectomized 3-4 weeks prior to implantation of a cannula into the third ventricle 1 week before the experiments. The day after implantation of an external jugular catheter, blood samples (0. 3 ml) were collected just before and every 10 min for 2 hr after 3V injection of 5 microl of diluent or 10 microg of leptin. Both doses of estradiol benzoate equally decreased plasma LH concentrations and pulse amplitude, but there was a graded decrease in pulse frequency. In contrast, only the 50-microg dose of estradiol benzoate significantly decreased mean plasma FSH concentrations without significantly changing other parameters of FSH release. The number of LH pulses alone and pulses of both hormones together decreased as the dose of estrogen was increased, whereas the number of pulses of FSH alone significantly increased with the higher dose of estradiol benzoate, demonstrating differential control of LH and FSH secretion by estrogen, consistent with alterations in release of luteinizing hormone releasing hormone (LHRH) and the putative FSH-releasing factor (FSHRF), respectively. The effects of intraventricularly injected leptin were drastically altered by increasing doses of estradiol benzoate. There was no significant effect of intraventricular injection of leptin (10 microg) on the various parameters of either FSH or LH secretion in ovariectomized, oil-injected rats, whereas in those injected with 10 microg of estradiol benzoate there was an increase in the first hr in mean plasma concentration, area under the curve, pulse amplitude, and maximum increase of LH above the starting value (Deltamax) on comparison with the results in the diluent-injected animals in which there was no alteration of these parameters during the 2 hr following injection. The pattern of FSH release was opposite to that of LH and had a different time-course. In the diluent-injected animals, probably because of the stress of injection and frequent blood sampling, there was an initial significant decline in plasma FSH at 20 min after injection, followed by a progressive increase with a significant elevation above the control values at 110 and 120 min. In the leptin-injected animals, mean plasma FSH was nearly constant during the entire experiment, coupled with a significant decrease below values in diluent-injected rats, beginning at 30 min after injection and progressing to a maximal difference at 120 min. Area under the curve, pulse amplitude, and Deltamax of FSH was also decreased in the second hour compared to values in diluent-injected rats. In contrast to the stimulatory effects of intraventricular injection of leptin on pulsatile LH release manifest during the first hour after injection, there was a diametrically opposite, delayed significant decrease in pulsatile FSH release. This differential effect of leptin on FSH and LH release was consistent with differential effects of leptin on LHRH and FSHRF release. Finally, the higher dose of E2 (50 microg) suppressed release of both FSH and LH, but there was little effect of leptin under these conditions, the only effect being a slight (P < 0.04) increase in pulse amplitude of LH in this group of rats. The results indicate that the central effects of leptin on gonadotropin release are strongly dependent on plasma estradiol levels. These effects are consistent w     

The effects of alpha 1-adrenergic and muscarinic cholinergic stimulation on prostaglandin release by rabbit iris

We have investigated the effects of norepinephrine (NE) and acetylcholine (ACh) on prostaglandin (PGE2 and 6 keto-PGF1 alpha) production by rabbit iris, measured by radioimmunoassay (RIA), and the type of phospholipase activated by NE in irides in which phosphatidylinositol (PI) was doubly prelabeled with [3H] myo-inositol and [1-14C] arachidonic acid (14C-AA), quantitated by radiometric and chromatographic methods. PGE2 output in 60 min (3.6 micrograms/g tissue) was 2.6 times greater than 6 keto-PGF1 alpha. PG production is time-dependent and it is stimulated by NE and ACh in a dose-dependent manner. The NE- and ACh-induced release of PGE2, measured by RIA, is mediated through alpha 1-adrenergic and muscarinic cholinergic receptors, respectively, and it requires Ca2+ for maximal stimulation. Studies on the mechanism of AA release from PI in irides doubly prelabeled with 14C-AA and [3H] myo-inositol revealed the following: (a) Both NE and ACh increased the breakdown of PI, and this was accompanied by a significant increase in the release of AA and consequently PGE2. The stimulatory effects of NE and ACh are mediated through alpha 1-adrenergic and muscarinic cholinergic receptors respectively. (b) The NE-induced formation of 3H-lyso PI and the NE-induced metabolism of 14C-1,2-diacyl-glycerol (DG) are time-dependent. Two pathways for AA release from PI are probably operative in the iris: (a) An indirect release by PI-specific phospholipase C which produces DG, followed by the actions of DG- and monoacylglycerol lipases on DG to release AA. (b) A direct release by phospholipase A2. Whether lyso PI is a product of the polyphosphoinositide response remains to be established. Other phospholipids such as phosphatidylcholine and phosphatidylethanolamine could also serve as a source for AA in PG synthesis. In conclusion, the data presented provide evidence that in the iris the neuro-transmitter-stimulated release of PG and AA, from phosphoinositides, for PG synthesis is coupled to the activation of alpha 1-adrenergic and muscarinic cholinergic receptors.     

The effects of alpha1-adrenergic and muscarinic cholinergic stimulation on prostaglandin release by rabbit iris

We have investigated the effects of norepinephrine (NE) and acetylcholine (ACh) on prostaglandin (PGE₂ and 6 keto-PGF_1α) production by rabbit iris, measured by radioimmunoassay (RIA), and the type of phospholipase activated by NE in irides in which phosphatidylinositol (PI) was doubly prelabeled with [³H] myo-inositol and [1-¹⁴C] arachidonic acid (¹⁴C-AA), quantitated by radiometric and chromatographic methods. PGE₂ output in 60 min (3.6 μg/g tissue) was 2.6 times greater than 6 keto-PGF_1α. PG production is time-dependent and it is stimulated by NE and ACh in a dose-dependent manner. The Ne- and ACh-induced release of PGE₂, measured by RIA, is mediated through α₁-adrenergic and muscarinic cholinergic receptors, respectively, and it requeires Ca²⁺ for maximal stimulation. Studies on the mechanism of AA release PI in irides doubly prelabeled with ¹⁴C-AA and [³H] myo-inositol revelased the following: (a) Both Ne and ACh increased the breakdown of PI, and this was accompanied by a significant increase in the release of AA and consequently PGE₂. The stimulatory effects of NE and ACh are mediated through α₁-adrenergic and muscainic cholinergic receptors respectively. (b) The NE-induced formation of ³H-lyso PI and the NE-induced metabolism of ¹⁴C-1,2-diacyl-glycerol (DG) are time-dependent. Two pathways for AA release from PI are probably operaitve in the iris: (a) An indirect release by PI-specific phospholipase C which producers DG, followed by the actions of DG- and monoacylglycerol lipases on DG to release AA. (b) A direct release by phospholipase A₂. Whether lyso PI is a product of the polypholipids such as prosphatidylcholine and phosphatidylethanolamine could also serve as a source for AA in PG synthesis. In conclusion, the data presented provide evidence that in the iris the neurotransmitter-stimulated release of PG and AA, from phosphoinositides, for PG synthesis is coupled to the activation of α₁-adrenergic and muscarinic cholinergic receptors.     

Effects of ovariectomy and estradiol replacement on naloxone induced LH secretion in the female rabbit

The effects of an opioid antagonist, naloxone, on the secretion of gonadotrophins were investigated in the long term ovariectomized rabbit. In the intact and acutely ovariectomized rabbit (2 days p.o.) naloxone at 10 mg/kg induced an increase of 260-300% in LH secretion at 40 min post-injection. From days 33-66 post-surgery naloxone at 10 mg/kg caused significant elevations in LH release even when animals were treated with estradiol benzoate 24 h previously. By contrast, treatment with oestradiol benzoate 3 h before naloxone abolished the LH increase. An LH surge could be elicited in these rabbits with GnRH treatment. These studies indicated that long term ovariectomy in the female rabbit does not completely remove the opioid control of GnRH release and that the LH response to naloxone is influenced by circulating estradiol levels.     

Norepinephrine-like effects of neuropeptide Y on LH release in the rat

Neuropeptide Y, a recently isolated neuropeptide exhibited norepinephrine-like effects on LH release after intracerebroventricular administration at doses from 0.5 to 10 micrograms. While it promptly suppressed LH release in ovariectomized rats, there was a dose-related stimulation of LH secretion in ovarian steroid primed-ovariectomized rats. In view of the evidence that neuropeptide Y may coexist with adrenergic neurotransmitters, these findings suggest that it may play a role in regulation of LH release in the rat, either independently or in concert with catecholamines.     

Effect of food deprivation on the pulsatile LH release in the cycling and ovariectomized female rat

The effect of food deprivation on the pulsatile release of LH was examined in the normal cycling and the ovariectomized (OVX) adult female rat. In the cycling animals, there were significant decreases in the mean plasma LH levels as well as the frequency and amplitude of the LH pulse 48 h after the onset of food deprivation. On the other hand, food deprivation for up to 72 h did not cause any changes in pulsatile LH release in the OVX animals. No difference in the changes in body weight and blood glucose concentration were found between the cycling and OVX rats throughout the period of food deprivation for up to 96 h. These findings suggest that ovarian factors play an important role in the early manifestation of the effect of food deprivation on pulsatile LH release and that metabolic changes as expressed by decreases in body weight and blood glucose level per se were not the direct causes in the decrease of LH release during the period of food deprivation.     

The effects of female choice and male-male competition on the mating success of male guppies

This study examined the effects of female choice and male-male competition on male mating success in the guppy, Poecilia reticulata. The fraction of a male's displays that elicited a sexual response from a female was used as a measure of relative female preference for that male. Male mating success was measured by scoring paternity of sons, using colour pattern as a genetic marker. Female preference had a significant effect on male mating success. Male-male competition was relatively uncommon, and did not involve direct threats or combat. Data on male-male competition did not significantly predict mating success. Males from different experimental groups with the same colour pattern had similar mating success. This suggests that female choice could have been based on colour pattern. However, there was no obvious relationship of particular colour pattern elements to mating success or female preference. The males with the same colour pattern were related and most were reared together, so other genetic or environmental factors could have led to similar mating success.     

The effects of indomethacin on plasma LH levels in female and male deermice ( )

The purpose of this investigation was to determine (1) the approximate time of the preovulatory LH rise in cyclic deermice, (2) the effect of indomethacin administration on plasma LH levels during the expected preovulatory LH rise, and (3) the effect of indomethacin administration on plasma LH levels in castrated male deermice. The data indicate that the preovulatory LH rise occurred at about 2200 h on proestrus and that indomethacin pretreatment significantly reduced plasma LH levels during that time. In addition, indomethacin significantly reduced plasma LH levels in castrated male deermice. We conclude that plasma LH levels remain low throughout the estrous cycle with the exception of the preovulatory “surge”, that plasma LH levels in deermice are comparable to those reported for the rat, and that indomethacin pretreatment reduced plasma LH levels during periods when they were expected to be elevated (in castrated males and during the expected preovulatory LH rise in female deermice). The data are consistent with the hypothesis that the effect of indomethacin on plasma LH levels is due to an inhibitory effect on hypothalamic PG biosynthesis.     

The feedback of exogenous steroids on LH release and ovulation in the intact female vole (Microtus agrestis).

Female voles were subjected to various regimens of subcutaneous injections of oestradiol-17beta, oestradiol benzoate and/or progesterone. Ovulation occurred in only a few of the mature females and in none of the immature animals. There was no indication of any increased LH levels in blood samples taken every 2 h for 50 h after 150 microgram oestradiol-17beta.     

Comparison between the biological effects of LH-RH and buserelin on the induction of LH release from hemi-pituitary glands of female rats in vitro

The biological effects of LH-RH and the agonist [D-Ser(But)6-des Gly10]-LH-RH(1-9)-ethylamide (buserelin) were compared during 8 h of incubation with female rat hemi-pituitary glands. Similar dose-response relationships were found for LH-RH and buserelin as concerns the release of luteinizing hormone (LH) by pituitary glands from intact and ovariectomized rats. Also the LH secretion patterns from glands of intact rats were similar: an initial low response was followed by a fast increase (priming effect) after which the response declined again (desensitization). In a subsequent experiment pituitary glands from ovariectomized rats were first exposed to LH-RH or buserelin for 4 h and then further incubated in medium only. After discontinuation of the stimuli the rate of LH release decreased in all cases, but this decrease was significantly greater when the glands had been exposed to LH-RH. Short-term (1/2, 1 or 2 h) exposures to LH-RH or buserelin followed by an intervening period (1 1/2, 1 or 0 h, respectively) of incubation in medium only resulted in an almost similar, significant increase in the subsequent protein synthesis-independent LH response to LH-RH (priming effect). Only preincubation with LH-RH for 2 h was significantly more effective. The results demonstrate equal intrinsic activities for LH-RH and buserelin. Differences in the biopotencies for LH-RH and buserelin in vivo and in vitro may occur only after discontinuation of the external stimuli.     

The influence of changes in tension on protein synthesis and prostaglandin release in isolated rabbit muscles.

Intermittent stretching of isolated rabbit muscles increased the rate of protein synthesis by 70% and prostaglandin-F2 alpha release by 105%. Both effects of intermittent stretching were blocked by indomethacin and meclofenamate; the absence of Ca2+ together with added EGTA also inhibited both processes. The residual influence of intermittent stretching on protein synthesis was closely correlated with prostaglandin-F2 alpha release, which may be the link between mechanical activity and protein synthesis in skeletal muscle.     

The effects of prey lipid on female mating and reproduction of a wolf spider

As predators, the macronutrients spiders extract from their prey play important roles in their mating and reproduction. Previous studies of macronutrients on spider mating and reproduction focus on protein, the potential impact of prey lipid content on spider mating and reproduction remains largely unexplored. Here, we tested the influence of prey varying in lipid content on female mating, sexual cannibalism, reproduction, and offspring fitness in the wolf spider Pardosa pseudoannulata. We acquired 2 groups of fruit fly Drosophila melanogaster that differed significantly in lipid but not protein content by supplementing cultural media with a high or low dose of sucrose on which the fruit flies were reared (HL: high lipid and LL: low lipid). Subadult (i.e., 1 molt before adult) female spiders that fed HL flies matured with significantly higher lipid content than those fed LL flies. We found that the mated females fed with HL flies significantly shortened pre-oviposition time and resulted in a significantly higher fecundity. However, there was no significant difference in female spiders varying in lipid content on other behaviors and traits, including the latency to courtship, courtship duration, mating, copulation duration, sexual cannibalism, offspring body size, and survival. Hence, our results suggest that the lipid content of prey may be a limiting factor for female reproduction, but not for other behavioral traits in the wolf spiders P. pseudoannulata.     

The effects of age at mating on female life-history traits in a seed beetle

Age at first reproduction is an important component of lifehistory across taxa and can ultimately affect fitness. Becausegenetic interests of males and females over reproductive decisionscommonly differ, theory predicts that conflict may arise overthe temporal distribution of matings. To determine the potentialfor such sexual conflict, we studied the direct costs and benefitsassociated with mating at different times for females, usingseed beetles (Acanthoscelides obtectus) as a model system. Virginfemales were resistant to male mating attempts at a very earlyage but subsequently reduced their resistance. Although we foundno difference in life span or mortality rates between femalesmated early in life and those mated later, females that matedearly in life suffered a 12% reduction in lifetime fecundity.Thus, there are direct costs associated with mating early inlife for females. Yet, males mate even with newly hatched females.We suggest that these data indicate a potential for sexual conflictover the timing of first mating and that female resistance tomating, at least in part, may represent a female strategy aimedat delaying mating to a later time in life.     

Gonadotropin release as a function of mating and steroid feedback in the female rat

The aim of this investigation was to study possible relationships between mating-induced and steroid-induced luteinizing hormone (LH) release in spayed Long-Evans rats. Large amounts of LH were released approximately 7 hr following progesterone injection in rats primed with estradiol benzoate (EB). The amount of LH release varied widely depending on (1) the interval between the time of the progesterone injection and the EB priming; (2) the progesterone dose; and (3) the time of day when blood samples were collected. These findings provided confirmation of those of Caligaris, Astrada and Taleisnik (1971a). Females, prepared with estrogen-progesterone treatment in a variety of schedules in which the three above-mentioned variables were altered systematically, were allowed to mate with vigorous males. Mating under these various conditions did not significantly increase plasma LH levels even when the females showed high degrees of sexual receptivity. Sodium pentobarbital prevented the afternoon LH rise resulting from progesterone treatment 3 days after EB priming. Pituitary sensitivity to LRF was not enhanced in the afternoon and the mating did not significantly increase plasma LH in these barbiturate-blocked rats. Following administration of 5 large daily doses of EB without progesterone, however, significant increases in LH were produced by mating on the sixth day. Postcopulatory LH release in these circumstances was dependent on a diurnal factor since the effect of mating was greater in the afternoon than in the morning. Thus, although major LH release can be readily induced by mating in estrogen-treated spayed rats, this effect could not be obtained under conditions of progesterone administration to estrogen primed rats.     

The effects of prenatal PCBs on adult female paced mating reproductive behaviors in rats

Polychlorinated biphenyls (PCBs) are a family of toxicants that persist in measurable quantities in human and wildlife tissues, despite their ban in production in 1977. Some PCB mixtures can act as endocrine disrupting chemicals (EDCs) by mimicking or antagonizing the actions of hormones in the brain and periphery. When exposure to hormonally active substances such as PCBs occurs during vulnerable developmental periods, particularly prenatally or in early postnatal life, they can disrupt sex-specific patterning of the brain, inducing permanent changes that can later be manifested as improper sexual behaviors. Here, we investigated the effects of prenatal exposure to the PCB mixture Aroclor (A) 1221 on adult female reproductive behaviors in a dose-response model in the Sprague-Dawley rat. Using a paced mating paradigm that permits the female to set the timing of mating and control contact with the male during copulation, we were able to uncover significant differences in female-typical sexual activities in A1221-exposed females. Specifically, A1221 causes significant effects on mating trial pacing, vocalizations, ambulation and the female's likelihood to mate. The results further demonstrate that the intermediate treatment group has the greatest number of disrupted endpoints, suggestive of non-linear dose responses to A1221. These data demonstrate that the behavioral phenotype in adulthood is disrupted by low, ecologically relevant exposures to PCBs, and the results have implications for reproductive success and health in wildlife and women.     

Effects of crude and pure cholera toxin on prostaglandin release from the rabbit ileum

Investigations were made into the effects of crude and pure preparations of cholera toxin on the release of prostaglandin-like substances (PLS) from rabbit ileum. Perfusion of ileal loops with buffer containing crude toxin was followed by a release of PLS into the perfusate, in amounts up to 37.5 ng/30 min (PGE₂ equivalents). In contrast, no detectable PLS was released when ileal loops were perfused with pure toxin. Similarly, pieces of ileum opened longitudinally released PLS in amounts up to 107 ng PGE₂/g tissue when incubated with crude toxin for 1–4 hr, but no release of PLS was detected in the presence of pure toxin under comparable conditions.Treatment of rabbits with indomethacin, 1.6 mg/kg p.o., had no effect on the accumulation of fluid in ileal sacs injected with crude or pure cholera toxin. These results support the view that prostaglandins do not play an essential role in the action of cholera toxin.