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PubMed1984

Effects of benztropine mesylate on haloperidol-induced prolactin secretion and serum haloperidol levels in rats.

The effects of benztropine mesylate on haloperidol-induced prolactin secretion and serum haloperidol levels were investigated in 240 rats. Animals were pretreated with benztropine mesylate or saline 20 min prior to receiving haloperidol or saline. Serum prolactin and haloperidol levels were analyzed at six time periods over 150 min. There was no significant difference in prolactin levels of control animals, i.e., saline pretreated/saline treated rats compared to benztropine mesylate pretreated/saline treated rats. Haloperidol caused a significant rise (p less than 0.0001) in serum prolactin compared with controls. The prolactin concentration for the 30-150-min sampling period was significantly higher when the rats received benztropine mesylate prior to haloperidol (p less than 0.05). There was a significant correlation (r = 0.57, p less than 0.001) between serum haloperidol levels and serum prolactin levels in haloperidol-treated animals pretreated with either saline or benztropine mesylate. Additionally, serum haloperidol levels were not significantly different in animals pretreated with benztropine mesylate compared with those pretreated with saline. Thus, the enhancement of prolactin levels by benztropine mesylate was independent of any effect of haloperidol metabolism. This study appears to indicate that in the rat, cholinergic mechanisms exert a weak inhibitory effect on prolactin secretion under conditions of dopamine blockade.

Animals↗
PubMed2000

A conspecific attenuates prolactin responses to open-field exposure in rats.

Acute exposure to a novel environment, such as an open field, generally results in a prolactin surge, while several days of exposure to the open field is often characterized by a decline in prolactin. As exposure to the open field is a psychological stressor, altering the animal's interpretation of the event should alter prolactin levels. In the present study, juvenile male and female rats were habituated to the open field for 1 or 5 days prior to testing in the chamber alone or with a same-sex conspecific. Levels of prolactin were measured across all rats, and play (pins) was recorded for animals tested with a conspecific. Five days of habituation to the chamber resulted in lower levels of prolactin and more play than 1 day of habituation. Across both conditions of habituation, testing with a conspecific caused lower levels of prolactin than testing alone. In addition, play and prolactin were negatively correlated. The presence of a conspecific in a stressful situation may have reduced stress by altering the animal's negative interpretation of the open field. Further, as the intensity of the social interaction increased (more play), prolactin levels decreased.

Animals↗
PubMed1976

Effects of selective sleep deprivation on sleep-linked prolactin and growth hormone secretion.

1. The secretion of prolactin and growth-hormone (hGH) was investigated during sleep in 10 healthy volunteers (8 males and 2 females): The comparison of one baseline night, one night after daytime physical exercise, and one night with selective deprivation of sleep stages 3 and 4 and paradoxical sleep showed clear differences of prolactin and hGH secretion during sleep. 2. Prolactin secretion is entrained into the sleep cycle of Non-REM and REM periods. A maximum of plasma hormone elevations occurs during the first quarter of sleep cycles, i.e., during Non-REM periods and less frequent rises at the end of the cycles, mainly during REM periods. 3. In contrast to growth hormone, concentrations of prolactin remain high also during later cycles occurring toward morning. This shows that high prolactin, but not high concentrations of hGH, regularly occur during sleep cycles with small amounts of slow-wave sleep. 4. Maximal prolactin concentrations during sleep are affected neither by preceding daytime physical exercise nor by selective deprivation of slow sleep stages 3 and 4. This is further evidence that slow-wave sleep stages are not necessary for the development of high plasma prolactin concentrations. However, peak values of growth hormone in the first and second cycle are significantly diminished after selective deprivation of sleep stages 3 and 4. 5. In abnormally long sleep cycles with artificial delay of the first REM period, the cyclical rhythmicity of prolactin release seems disturbed. This is further evidence for the sleep-dependent rhythmicity in the secretion of this hormone.

Adult↗
PubMed1992

Ultrastructural and cytochemical studies of the effects of prolactin on the lateral prostate and the seminal vesicle of the castrated guinea pig.

Administration of ovine prolactin to castrated guinea pigs for 2 weeks induced hypertrophy of secretory cells in the lateral prostate when compared with the castrated controls. This was accompanied by an apparent increase in the number of profiles of granular endoplasmic reticulum and well developed Golgi complexes with dilated cisternae. An increase in the number of low-contrast electron-dense secretory granules was observed 4 weeks after prolactin treatment. In the seminal vesicle, dilatation and degranulation of granular endoplasmic reticulum and an apparent decrease in the number of secretory granules were observed 4 weeks after prolactin administration. Following castration and 2 weeks after prolactin treatment, thiamine pyrophosphatase (TPPase)-reaction product was mainly confined to 1-2 trans cisternae of the Golgi complexes in secretory cells of the lateral prostate and the seminal vesicle. In both glands, a reduction of TPPase activity was observed 2 weeks following prolactin administration, and the reaction product was totally absent after prolonged treatment for 4 weeks. The present study has provided morphological evidence that prolactin is capable of stimulating the secretory function of the lateral prostate while exerting some inhibitory effects on the seminal vesicle of the castrated guinea pig. In both glands, TPPase activity, and hence the process of glycosylation was inhibited after prolactin administration. The results from radioimmunoassay indicated that the action of prolactin on these glands could be a direct effect and not mediated through testosterone.

Animals↗
PubMed1993

Effects of intraventricular taurine, homotaurine and GABA on serum prolactin and thyrotropin levels in female and in male rats.

Serum prolactin and thyrotropin levels of conscious, unrestrained male and female rats were compared after intracerebroventricular (i.c.v.) administration of taurine, gamma-aminobutyric acid (GABA) and homotaurine. The amino acids studied had no clear effect on serum basal thyrotropin levels in male or female rats. All amino acids elevated serum prolactin levels in female rats at the dose of 5 mumol/rat; homotaurine by about 18-fold, taurine and GABA by 3-fold. Only homotaurine elevated serum prolactin of male rats at this dose, but its effect was less pronounced (p < 0.01) in male than in female rats. Although homotaurine was clearly more potent than the two other amino acids, at the dose of 10 mumol/rat taurine and GABA also elevated serum prolactin in male rats. These findings show that there are gender-related differences in the responses of serum prolactin levels to homotaurine, taurine and GABA in rats. The tuberoinfundibular dopaminergic pathway, which exerts tonic inhibitory influence on prolactin secretion, is sexually differentiated. Hence the gender-related differences in the effects of the amino acids on prolactin secretion suggest that they might inhibit dopamine release from the median eminence. In case of homotaurine, the gender effect was most pronounced. The less clear dependence of GABA's effect on the gender is in accordance with the suggestions that GABA influences the secretion of serum prolactin by more than one mechanism.

Animals↗
PubMed2001

Severe lymphocytic adenohypophysitis with selective disappearance of prolactin cells: a histologic, ultrastructural and immunoelectron microscopic study.

We report the first documented example (case 1) of lymphocytic adenohypophysitis (LAH) associated with selective destruction of prolactin cells. The morphologic data are compared to those obtained in another, more typical case (case 2). Case 1 was a 35-year-old woman with remote history of pregnancy who presented with headache, oligomenorrhea and visual disturbances. The blood prolactin level was nearly undetectable, but no deficiency of other pituitary hormones was evident. A sellar and parasellar mass compressing the optic chiasm was removed transsphenoidally. Histology demonstrated massive infiltration with lymphocytes, plasma cells and macrophages causing marked destruction of pituitary acini. Part of the gland was fibrotic. Immunocytochemistry documented all pituitary hormones, but only few cells, probably mammosomatotrophs, were immunoreactive for prolactin. Electron microscopy and immunoelectron microscopy using double gold labeling for growth hormone and prolactin detected no prolactin cells. A striking ultrastructural finding was the prominence of folliculostellate cells in areas of active cell destruction supporting the presumed immune role of these cells. LAH in case 2 (24-year-old woman) became manifest during late pregnancy, causing pituitary enlargement and visual field defects. Pituitary tests showed no major hormonal deficits. Moderate hyperprolactinemia was appropriate for her pregnancy status. A sellar mass, thought to be adenoma, was removed. Histology demonstrated multifocal LAH without major destruction of acinar structures. Immunocytochemistry and electron microscopy documented all pituitary cell types including the marked abundance of prolactin-producing cells, resultant of gestational prolactin cell hyperplasia. In addition to prolactin cells and growth hormone cells, immunoelectron microscopy showed several bihormonal mammosomatotrophs, also appropriate for pregnancy.

Adult↗
PubMed1987

Misinterpretation of prolactin levels leading to management errors in patients with sellar enlargement.

Serum prolactin concentrations and clinical features were correlated with the histopathologic diagnosis in 128 patients, without acromegaly or Cushing's syndrome, referred for surgical treatment of a presumed pituitary adenoma. A serum prolactin concentration of more than 8,000 mU/liter was always due to a prolactin-secreting adenoma. Prolactin levels of less than 8,000 mU/liter occurred with a variety of pathologic diagnoses. Fifteen patients had lesions other than pituitary adenomas, most commonly intrasellar craniopharyngioma; 10 of these had modest hyperprolactinaemia (maximum, 5,260 mU/liter) and four had received inappropriate bromocriptine therapy. Adenomas that were not prolactinomas frequently caused mild hyperprolactinaemia, although this was usually less than 3,000 mU/liter; three of these patients, however, had serum prolactin concentrations greater than this (maximum, 8,000 mU/liter). If the serum prolactin concentration is less than 3,000 mU/liter in the presence of significant pituitary enlargement, surgical removal is essential for both diagnosis and treatment since only prolactin-secreting adenomas are likely to shrink with dopamine agonist therapy. A serum prolactin concentration between 3,000 and 8,000 mU/liter is consistent with any diagnosis, whether the fossa is greatly enlarged or not, and great care must be taken with dopamine agonist therapy in such patients.

Adenoma↗
PubMed1983

Prolactin secretion by human chorion-decidua in vitro: influences of mode of delivery and agents that modify prostaglandin synthesis.

Prolactin production by human decidua was examined with the use of a short-term tissue explant system. Decidua obtained after normal spontaneous vaginal deliveries produced significantly more prolactin than did tissue obtained after elective repeat cesarean section deliveries in the absence of labor (P less than 0.005). Cytosolic prolactin levels did not differ between the two delivery modes. Oxytocin (4.3 X 10(-11) M to 4.3 X 10(-6) M) and eicosatetraenoic acid (10(-7) M to 10(-4) M) had no effect on prolactin production or storage by decidual tissue. Indomethacin at 10(-4) M reduced only levels of stored prolactin but had no effect on stored or produced prolactin at lower concentrations (10(-7) M to 10(-5) M). Arachidonic acid (10(-4) M) suppressed both production and storage of prolactin (P less than 0.05). Decidual tissue from the two delivery modes did not differ in response to the above agents. Although the exact mechanism(s) remains obscure, these results indicate decidual prolactin production is altered by some aspect of labor. The possible involvement of prostaglandin precursors in mediating this production cannot be excluded.

Arachidonic Acids↗
PubMed1985

Prolactin production by explants of normal, luteal phase defective, and corrected luteal phase defective late secretory endometrium.

The production of prolactin by explants of late secretory endometrium has been correlated with the extent of decidual differentiation. This correlation is strengthened by the observation that luteal phase defective endometrium produces less prolactin than normal control endometrium in a 24-hour in vitro culture system. In the present study the prolactin production by explants of normal, luteal phase defective, progesterone-corrected luteal phase defective, and clomiphene- or follicle-stimulating hormone/luteinizing hormone-corrected luteal phase defective late secretory endometrium was measured over 96 hours at 24-hour intervals. Progesterone in physiologic concentrations was added to the culture medium to maintain tissue integrity and prolactin synthesis. The prolactin production of normal late secretory endometrium rose over 96 hours under progesterone stimulation. The luteal phase defective endometrium produced significantly less prolactin under the same conditions. Histologically proven corrected luteal phase defective endometrium, regardless of treatment method, produced prolactin not different from the normal controls of the same dates. From these results it is concluded that histologic correction of luteal phase defective endometrium is associated with a corresponding biochemical correction with use of prolactin as a metabolic marker. The findings also strongly support timed endometrial biopsy as the method of diagnosis and evaluation of treatment of luteal phase defect.

Biopsy↗
PubMed1988

Influence of preovulatory estradiol concentration on diurnal and pulsatile prolactin secretion patterns.

We evaluated the effect of preovulatory concentrations of estradiol on the 24-hour profile of prolactin secretion in women with regular menstrual cycles. An estradiol preparation was chosen to allow comparison with physiologic events. Estradiol benzoate, 1 mg intramuscularly, was administered for 7 days to achieve estradiol concentrations just above preovulatory levels (424 +/- 54 pg/ml); 24-hour mean prolactin concentrations increased threefold (14.0 +/- 2.1 to 40.6 +/- 7.1 ng/ml). Prolactin pulse frequency increased significantly (p less than 0.001) during waking hours after estradiol benzoate administration. The diurnal pattern of prolactin secretion was maintained with estradiol benzoate, although the sleep acrophase often reached high concentrations (86 +/- 11 ng/ml). These results suggest in women with regular menstrual cycles: (1) that estrogen administration that achieves slightly greater than preovulatory estradiol concentrations can stimulate prolactin release, (2) that estradiol may elevate prolactin by increasing its pulsatile secretion, (3) that estradiol does not alter the diurnal pattern of prolactin secretion, (4) that estradiol concentrations just above preovulatory levels can be associated with markedly elevated prolactin concentrations.

Adult↗
PubMed1991

A selective serotonin reuptake inhibitor, fluoxetine hydrochloride, modulates the pulsatile release of prolactin in postmenopausal women.

We investigated serotoninergic regulation of prolactin release in estrogen-withdrawn postmenopausal women by using a serotonin reuptake inhibitor. Subjects underwent frequent blood sampling after placebo (basal) or fluoxetine administration. Mean 24-hour serum prolactin concentrations increased significantly in response to fluoxetine. Objective pulse analysis revealed no change in prolactin pulse frequency with serotoninergic stimulation, but maximal serum prolactin peak heights increased significantly. Multiple-parameter deconvolution disclosed no change in prolactin half-life, but a significant increase in the total mass of prolactin secreted per 24 hours during fluoxetine administration. Cosinor analysis of the prolactin time series showed a significant increase in the circadian amplitude and mean without any change in the time of maximal concentration during treatment with fluoxetine. We conclude that short-term activation of the serotoninergic system in the absence of substantial estradiol and opiatergic tone significantly increases the secretion of prolactin in postmenopausal women.

Circadian Rhythm↗
PubMed1986

Modulation of prolactin binding sites in vitro by membrane fluidizers. IV. Differential effects on plasma membrane and Golgi fractions of male prostate and female liver in the rat.

In vitro treatment of crude particulate fractions of male rat ventral prostate and female rat liver with membrane fluidizers (aliphatic alcohols) has been previously reported by us to increase prolactin (PRL) receptor levels, presumably by unmasking cryptic prolactin receptors. The objective of this study was to determine if similar in vitro treatment of purified plasma membrane- and Golgi-rich fractions of male rat prostate and female rat liver with ethanol produced differential effects on prolactin binding in these two subcellular fractions. The degree of fluidization was monitored by a fluorescence polarization method using 1,6-diphenylhexatriene. 125I-PRL specific binding to Golgi-rich fractions of male ventral prostate and female liver was approximately 4-fold higher than that observed in plasma membrane-rich fractions. The microviscosity parameter, inversely related to lipid fluidity, was consistently lower in Golgi-rich fractions than that in plasma membrane-rich fractions in both prostate and liver. In vitro ethanol treatment of prostatic and hepatic plasma membrane fractions produced a dose-related increase and then decline in prolactin binding and a maximal (60-75%) increase in prolactin binding was observed at 4.8% and 2.0% ethanol in prostatic and hepatic membranes, respectively. This in vitro treatment also produced a significant increase in apparent lipid fluidity of plasma membrane-rich fractions of prostate gland and liver. However, similar in vitro ethanol treatment of Golgi fractions of both prostate gland and liver exhibited little increase in prolactin binding without changing microviscosity. Our observations are consistent with the direct relationship between membrane fluidity and prolactin receptor levels. The changes in prostatic and hepatic plasma membrane fractions following in vitro ethanol treatment suggest that prolactin receptors located on the plasma membranes may be modulated (via membrane lipid microviscosity changes) in vivo to a greater extent by various physiological agents than those located within the Golgi fraction.

Animals↗
PubMed1977

Prolactin in human and rat serum and cerebrospinal fluid.

Rats treated with haloperidol or bearing subcutaneous implants of prolactin-secreting tumors had elevated CSF prolactin levels compared to those observed in control rats. These levels were commensurate with the increased serum level of prolactin, although there appeared to be an upper limit to the CSF prolactin concentration. Patients with prolactin-secreting pituitary adenomas had elevated CSF hormone levels as compared to patients with non-endocrine neurologic disease. This obtained, regardless of whether the tumor was intra- or extrasellar in its growth. The implications for the route of entry of prolactin into CSF under both normal and abnormal conditions, and the potential role for CSF prolactin as part of a feedback regulatory system on pituitary prolactin release are discussed.

Adenoma↗
PubMed1982

Catecholamine mechanisms in medio-basal hypothalamus influence prolactin but not growth hormone secretion.

Medio-basal hypothalamic (MBH) catecholamine mechanisms in the regulation of prolactin and growth hormone (GH) secretion were investigated in unanesthetized rats with chronic indwelling venous cannulae and bilateral MBH directed intracerebral guide cannulae. MBH injections of the catecholamine-specific neurotoxin 6-hydroxydopamine (6-OHDA; 2 micrograms base in 0.5 microliter 0.9% saline) had no effect upon basal prolactin or GH secretion. Examination of catecholamine fluorescence indicated that MBH 6-OHDA treatment produced widespread disruption of MBH catecholamine afferents but did not destroy tuberoinfundibular dopamine neurons of the arcuate nucleus, nor median eminence catecholamine structures. MBH injections (0.5 microliter, 0.032 M solutions) of dopamine, noradrenaline or adrenaline all produced statistically significant increases in plasma prolactin levels. The potency of these 3 catecholamines in evoking prolactin release differed markedly, adrenaline having the greatest effect. MBH catecholamine injections had no effect upon plasma GH levels compared to saline injected controls. The present data suggest that MBH catecholamine afferents are unimportant in the regulation of basal patterns of GH or prolactin secretion. As MBH catecholamine injections stimulate prolactin release this region may contain a prolactin-facilitatory catecholamine mechanism which is capable of generating prolactin surges in response to certain environmental or endogenous stimuli.

Animals↗
PubMed1988

Morphine does not stimulate prolactin release during lactation.

The ability of morphine to stimulate prolactin and growth hormone (GH) release was investigated in male rats and in female rats during diestrus, proestrus and lactation. In agreement with previous reports, acute morphine administration produced an increase in circulating levels of prolactin in male and in diestrous and proestrous female rats. In contrast to these results, morphine administration (10 or 15 mg/kg, s.c.; 5 mg/kg, i.v.; 5 or 10 micrograms, i.c.v.) did not produce an increase in prolactin levels in lactating dams. Morphine stimulates prolactin release in part by decreasing dopamine turnover in the tuberoinfundibular neurons in the median eminence. In order to assess the functional activity of these neurons during lactation, haloperidol (0.1 or 0.5 mg/kg, i.v.) was given to lactating dams. There was a significant increase in prolactin levels following haloperidol administration, suggesting that these dopaminergic neurons are participating in the modulation of prolactin release during lactation. In contrast to the insensitivity of the lactating rat to morphine stimulation of prolactin release, the intraventricular administration of two other opiate receptor agonists, beta-endorphin (10 or 20 micrograms) and [D-Ala-D-Leu]enkephalin (DADLE; 5 or 10 micrograms), produced significant increases in circulating levels of this hormone. The GH response to morphine, beta-endorphin and DADLE was also measured in these same rats. All these opiate receptor agonists stimulated GH release in male rats and in female rats during diestrus and proestrus as well as during lactation. These observations suggest that the suckling stimulus during lactation renders the rat refractory to morphine stimulation of prolactin release, possibly as a result of down-regulation of the mu-opiate receptor subtype.

Animals↗
PubMed1991

Dopamine receptor and adrenoceptor agonists inhibit prolactin release from MMQ cells.

MMQ cells, a prolactin-secreting cell line possessing dopamine receptors, were exposed to the calcium channel activator maitotoxin and dopamine or adrenoceptor agonists or antagonists. Dopamine (500 nM) or the dopamine agonists lisuride (50 nM), terguride (50 nM), and N-0437 (50 nM) decreased maitotoxin-stimulated prolactin release from perifused MMQ cells. In this system, sulpiride (100 nM), a dopamine D2 antagonist, reversed the prolactin inhibition produced by lisuride (20 nM). In static incubations of MMQ cells, lisuride (10-500 nM) inhibited maitotoxin-stimulated prolactin release in a concentration-dependent manner; this inhibition was attenuated in a concentration-related manner by sulpiride (100-500 nM). In addition, sulpiride reversed dopamine (50-500 nM), lisuride (10-500 nM), and terguride (50-500 nM) inhibition of forskolin-stimulated cAMP generation. The alpha 2-adrenergic agonist clonidine inhibited maitotoxin-stimulated prolactin release from perifused MMQ cells; this inhibition was abolished by idazoxan, an alpha 2-adrenergic antagonist. In contrast, serotonin or the serotonin antagonist methysergide had no effect on prolactin release from MMQ cells. These data indicate that activation of dopamine D2 receptors and alpha 2-adrenoceptors by classically defined pharmacological agents inhibits prolactin release and cellular cAMP levels in MMQ cells. Therefore, MMQ cells may provide a valuable model for the development of pharmacological agents and assist in the identification of the mechanisms involved in the dopaminergic inhibition of prolactin release.

Adrenergic Agonists↗
PubMed1983

Effects of external Mg2+ and Ca2+ on branchial osmotic water permeability and prolactin secretion in the teleost fish Sarotherodon mossambicus.

In Sarotherodon mossambicus prolactin cell activity is related to ambient Ca2+ levels, and prolactin has hypercalcemic activity in this species. To study whether prolactin has a direct action on calcium metabolism, or whether prolactin's relationship with calcium is indirect and connected with control of gill permeability, the effects of external Ca2+ and Mg2+ on prolactin secretion and gill permeability were compared. It appeared that high external Mg2+ was associated with reduced prolactin secretion, even though high Mg2+ resulted in a marked hypocalcemia. Exposure of fish to high Ca2+ levels led to hypercalcemia. Both high Mg2+ and high Ca2+ concentrations in the ambient water reduced the osmotic water permeability of the gills. These results represent further evidence that prolactin secretion in S. mossambicus may be affected by any external factor that interferes with branchial permeability. It is concluded that prolactin's main function in this species is connected with control of branchial permeability rather than calcium metabolism, although internal calcium may be implicated in permeability control.

Animals↗
PubMed1983

Serum levels of luteinizing hormone (LH), prolactin, estradiol, and progesterone in laying and nonlaying canvasback ducks (Aythya valisineria).

Temporal changes in the levels of serum luteinizing hormone (LH), prolactin, estradiol, and progesterone associated with the reproductive patterns of 53 wild captive canvasback ducks were measured. The reproductive endocrinology of both laying and nonlaying females was compared in this 3-year study. Females that remained sexually inactive had ovaries with small, undeveloped follicles. Nonlaying ducks also had lower serum levels of LH (P less than 0.01), prolactin (P less than 0.05), estradiol, and progesterone than those of laying ducks in mid-April (during prelay), mid-May (on the fourth day of egg production), and mid-June (during postlay and incubation). Prolactin levels of both layers and nonlayers increased over this time interval (P less than 0.01) but levels of nonlayers were significantly lower than those of layers for the three blood-sampling dates. The low prolactin levels demonstrate that reproductive failure was not a result of inhibition by high serum prolactin levels. Intravenous injections of luteinizing hormone-releasing hormone (LHRH) in female canvasbacks resulted in significantly elevated (P less than 0.01) serum LH on the prelay blood sampling date. Lack of reproduction in nonbreeding canvasbacks was thus associated with low circulating serum LH levels but with LHRH-sensitive pituitary pools. These data suggest that lack of reproduction was a result of the failure of the hypothalamus to release releasing factors. The serum hormones of laying canvasbacks varied temporally with stages of the nesting cycle. LH levels increased prior to egg laying and fluctuated during the laying period. LH levels decreased at the onset of incubation but increased after loss of clutch, with renesting activity. Serum prolactin levels of layers were low prior to egg laying and increased gradually through laying of the first clutch, the renesting period, and laying of the second clutch. The highest prolactin levels occurred in ducks incubating their eggs. Prolactin levels decreased in ducks that failed to incubate their eggs. Serum estradiol levels increased sharply between 2 and 5 weeks prior to egg laying and remained high until the second day of egg production. Estradiol levels decreased when the fourth egg was produced, and remained low through the laying of the first clutch, the renesting period, and laying of the second clutch. Progesterone fluctuated widely through the nesting cycle, showing several major peaks before laying and another during incubation.

Animals↗