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PubMed1988

The distribution of progesterone receptor in the 20-day-old fetal mouse: an autoradiographic study with [125I]progestin.

The distribution of progestin target sites in 20-day-old fetuses of estrogen-primed pregnant mice was investigated by thaw-mount autoradiography. Pregnant mice received a Silastic estradiol implant on day 17 and were ovariectomized on day 19 of pregnancy. Twenty-four hours after ovariectomy 10 prematurely delivered fetuses were each injected with 0.33 microgram/100 g BW [125I]progestin (SA, 2200 Ci/mM). To show specificity of progestin localization two additional fetuses were each injected sc with 20 micrograms R5020, a synthetic progestin, 1 h before the injection of [125I]progestin. The fetuses were frozen 2 h after injection of [125I]progestin, sectioned, and processed for thaw-mount autoradiography. Cells with nuclear uptake and retention of radioactivity were observed in numerous tissues, including certain regions of the oral mucosa and developing teeth, esophagus, larynx, skin, mammary gland, skeletal muscle, kidney, and reproductive glands and ducts. Injection of unlabeled R5020 1 h before [125I]progestin prevented nuclear concentration of radioactivity in all target tissues. The results indicate that progesterone receptors are expressed with a regional, cellular, and subcellular distribution in term fetal mouse tissues and suggest that progesterone is important to the growth and development of certain fetal tissues.

Affinity Labels↗

PubMed1979

Progestin binding in vitro by the brain cell nuclei of ovariectomized oestrogen-primed rats.

The uptake and binding of 17 alpha, 21-dimethyl-19-nor-4,9-pregnadiene-3,20-dione, a synthetic progestin, by the hypothalamus and cerebral cortex of ovariectomized oestrogen-primed rats was examined in vitro. Uptake of this steroid by the medial basal hypothalamus was higher than that by the remaining hypothalamus and cerebral cortex. The component in the cytosol from whole hypothalami which bound the radioactive progestin sedimented in the 7S region when centrifuged in a sucrose density gradient. The tritiated progestin was displaced by incubation with non-radioactive progestin or progesterone but not by oestradiol-17 beta, corticosterone or 5 alpha-dihydrotestosterone (1 mumol/l). No 7S binding component was detected in a similar preparation from the cerebral cortex. The nuclear fraction from whole hypothalami extracted by KCl (0.4 mol/l) contained a progestin-binding complex which sedimented at 9S and which was heat-labile and protein in nature. It was concluded that the hypothalamus of ovariectomized oestrogen-primed rats contains progestin-binding material in the cytoplasm and progestin, bound to such material, is transported from the cytoplasm to the nucleus.

Animals↗

PubMed2001

Control of reproduction with anti-progestin and oestrogens in captive bears.

The aim of this study was to establish new methods for controlling reproduction in bears. Anti-progestins were used to interrupt pregnancies. In two consecutive years, the anti-progestin J956 was administered to 11 female bears (nine Ursus arctos, one Ursus tibethanus, one Tremarctos ornatus) living in zoos. The anti-progestin J956 was given orally (n = 4) or parenterally (n = 12). The anti-progestin was administered alone or in combination with ethinyloestradiol, and before or after embryo implantation. The effects of anti-progestin treatment were determined using ultrasonographic examination of the urogenital tract and by monitoring progesterone concentrations in the blood and faeces. Oral administration of anti-progestin was not successful (successful in 0 of 4); however, in contrast, none of the parenteral treated animals remained pregnant (successful in 12 of 12). Parenteral treatment with J956, with or without ethinyloestradiol, was effective in disrupting pregnancy before implantation (successful in 6 of 6) and after implantation (successful in 6 of 6), but administration one month after implantation (n = 2) resulted in incomplete resorption of the fetuses. In conclusion, the administration of anti-progestins may be a useful method for preventing embryo implantation in captive bears.

Abortifacient Agents↗

PubMed2003

Progestins initiate adverse events of menopausal estrogen therapy.

OBJECTIVE: Recent report, particularly the Women's Health Initiative, demonstrated that hormone therapy with combined estrogen plus progestin increased the incidence of heart attacks, stroke, blood clots, breast cancer and dementia in women over 65 years old. We investigated the role of synthetic progestins in initiating the adverse events associated with estrogen therapy. METHODS: We used a fluorescence imaging technique, which allows video microscopic recordings of blood flow, blood vessel morphology and activities of various blood cells in a live animal. The acute peripheral and cerebrovascular responses were measured following intraperitoneal (5 or 10 mg) or intravenous (10 or 100 microg) administration of progesterone, synthetic progestins (medroxyprogesterone acetate and norethindrone) or estrogens (conjugated equine estrogens and 17 beta-estradiol). RESULTS: In both peripheral and cerebral vasculature, synthetic progestins caused endothelial disruption, accumulation of monocytes in the vessel wall, platelet activation and clot formation, which are early events in atherosclerosis, inflammation and thrombosis. Natural progesterone or estrogens did not show such toxicity. CONCLUSION: The risk associate with combined estrogen plus progestin therapy may be a consequence of vascular actions of progestins. Using progestins with minimal vascular toxicity may lead to safer estrogen preparations for menopausal women.

Animals↗

PubMed1986

Are cytosol estrogen and progestin receptors of prognostic significance in the management of epithelial ovarian cancers?

Cystosol estrogen and progestin receptor levels in tumor samples from 101 patients with previously untreated primary epithelial ovarian cancers were correlated with patient survival. Patients with stage I and II disease whose tumors contained elevated levels of cytosol progestin receptors had an improved survival over patients with tumors containing low levels of cytosol progestin receptors. However, patients with advanced ovarian cancers and low cytosol progestin receptors had significantly longer survival. The four-year estimated duration of survival with advanced disease and cytosol progestin receptors less than seven was 82%, whereas if the cytosol progestin receptors were seven or more, the four-year estimated duration of survival was only 10%. The explanation for this dichotomy is not evident at this time. In this study cytosol estrogen receptor levels were not associated with survival. These results suggest that measurement of cytosol progestin receptors is of prognostic value in advanced epithelial ovarian cancers.

Cytosol↗

PubMed1985

Effects of body weight, adrenal status, and estrogen priming on hypothalamic progestin receptors in male and female rats.

Some laboratories have reported sex differences in the effect of estrogen priming on neural progestin receptor concentration, whereas others find no such differences. The present studies sought to identify experimental variables which might differentially influence the measurable level of hypothalamic cytosol progestin receptors in adult male and female rats. The influence of three variables, body weight, adrenal status, and estrogen priming regimen, was evaluated. Treatment with low doses of estrogen (2 or 8 micrograms of estradiol benzoate (EB) 48 hr before sacrifice) was slightly but not significantly more effective in elevating hypothalamic progestin receptor content in age-matched females than in males despite the 40% greater body weights of males. When the same doses of EB were administered per 200 gm of body weight to animals with and without adrenal glands, both basal and estrogen-induced levels of hypothalamic progestin receptor were significantly higher in adrenalectomized/gonadectomized rats than in rats which were gonadectomized only, regardless of sex. There was no significant effect of sex or any interaction between sex, adrenal status, or estrogen priming dose. The only significant sex difference in brain progestin receptors occurred when weight-matched males and females received multiple injections of higher priming doses of estrogen (three daily injections of 10 micrograms of EB). Under these conditions, females showed up to 2-fold higher levels of hypothalamic progestin receptors than males, regardless of adrenal status. These data suggest that sex differences may exist in the neural progestin receptor systems of male and female rats, but the relationship of these differences to sex differences in neuroendocrine function or behavior is not clear.

Adrenal Glands↗

PubMed1982

Progestin receptor levels in rat hypothalamic and limbic nuclei.

We have utilized a method to minimize cytosol progestin receptor loss during freezing in order to localize the quantify estrogen-inducible progestin receptors in individual nuclei of the female rat brain. Ovariectomized females received estradiol benzoate (20 micrograms for 3 days) or vehicle prior to sacrifice. All animals were perfused with cold distilled H2O containing the cryoprotective compound, dimethyl sulfoxide (DMSO; 10% (v/v)). Thirty-one nuclei or brain regions were removed from frozen sections (300 micrometers) according to the method of Palkovits (Palkovits, M. (1973) Brain Res. 59: 449-450) and were assayed in vitro using a synthetic radioligand, [3H]R5020. In ovariectomized animals perfused with DMSO, a basal level (1 to 8 fmol/mg of protein) of progestin receptors was observed in a variety of preoptic, hypothalamic, and limbic structures. Moreover, estrogen treatment induced high levels (24 to 49 fmol/mg of protein) of progestin receptors in regions of the preoptic area of hypothalamus which contain high levels of estrogen receptors. These regions included the medial, periventricular, and superchiasmatic nuclei of the preoptic area, the periventricular anterior hypothalamus, the ventromedial nucleus, and the arcuate-median eminence. Moderate levels (2 to 8 fmol/mg of protein) of progestin receptors were induced by estrogen in other hypothalamic and limbic structures, including the anterior and lateral hypothalamus, the bed nucleus of the stria terminalis, the cingulate cortex, the medial amygdaloid nucleus, and the CA subfield of the hippocampus. By contrast, some areas, such as the caudate-putamen and the supraoptic nucleus, were devoid of both estrogen-inducible and uninduced progestin receptors. These results support the hypothesis that progesterone action in the central nervous system is mediated by cytosol receptors in discrete brain regions and provide the first quantitative map of progestin binding in a vertebrate brain.

Animals↗

PubMed1997

Progestins and breast cancer risk.

There is still no clear account on the role that progestins play in human breast cancer, and the issue continues to be debated. The effects of progestins on breast cell proliferation have been investigated in a number of different experimental systems with conflicting results. Progesterone has been reported to both stimulate and inhibit the growth of experimental mammary tumors, depending upon the dose and the experimental models. Epidemiological studies on the effect of combined hormone replacement therapy (HRT) on breast cancer risk in menopausal women are limited because the use of a progestin in addition to estrogens was not widely adopted until 10 years ago. Taking meta-analysis into account estrogen-progestin use did conclude that there is not an excess risk in combined HRT users. Epidemiological studies have provided conflicting results, ranging from a protective effect to a deleterious effect of progestin addition on breast cancer risk. Progestins include a large family of molecules characterised by different binding capacities to androgen receptors. This implies that they should be considered as distinct yet related, therapeutic agents. The use of different progestins may account for the controversial results obtained in studies conducted in different geographic areas.

Animals↗

PubMed1997

Effects of progestin administration on the hypothalamic-pituitary-adrenal axis and glucose homeostasis in dogs.

The effects of medroxyprogesterone acetate (MPA) and proligestone (PROL) on the hypothalamic-pituitary-adrenocortical axis and glucose homeostasis were studied in two groups of eight ovariohysterectomized beagle bitches. In addition, the binding characteristics of MPA and PROL for the progesterone and glucocorticoid receptor were investigated. The administration of both progestins resulted in suppression of the hypothalamic-pituitary-adrenal axis. Whereas basal plasma concentrations of adrenocorticotrophic hormone (ACTH) were only moderately affected, the basal plasma concentrations of cortisol and the cortisol:creatinine ratio in urine were significantly decreased after the first administration of both progestins. In the group given MPA the increase of ACTH after stimulation with corticotrophin-releasing hormone (CRH) remained normal but it was suppressed in the group treated with PROL. In both treatment groups the increase of cortisol after stimulation with CRH was lower. After cessation of progestin administration both basal and stimulated plasma ACTH concentrations returned to pretreatment concentrations within a few weeks. In contrast, it took 6 month to restore the basal plasma cortisol concentrations and cortisol:creatinine ratios in urine. Paradoxically, the stimulated cortisol concentrations returned to normal shortly after the cessation. Histological examinations revealed a severe atrophy of the zona fasciculata and reticularis of the adrenal gland in all treated dogs and a steroid-induced hepatopathy in 50% of them. During the first half of the progestin treatment, glucose homeostasis was maintained by increased plasma concentrations of insulin in both groups. After prolonged treatment the response to a glucose load became impaired. None of these parameters improved during the 6 month recovery period. Histological changes in the pancreas, characteristics of diabetes mellitus, were found in two dogs of each group. Most probably, the glucocorticoid action of the progestins is not the sole explanation for the insulin resistance since progestin treatment resulted in a concomitant increase in plasma concentrations of growth hormone which has diabetogenic properties. Experiments in vitro confirmed the strong glucocorticoid component of MPA and PROL. The inhibition constants (Ki) of PROL for both the progesterone receptor (PR) and the glucocorticoid receptor (GR) were approximately then times higher than those of MPA. Nonetheless, the ratios of the Ki for the GR and PR indicated that the specificity of MPA and PROL was only slightly different but considerably smaller than that of progesterone. It is long-term treatment with high doses of these progestins may result in a iatrogenic Cushing's syndrome and diabetes mellitus.

Adrenocorticotropic Hormone↗

PubMed1981

Treatment of advanced breast cancer with progestins.

This paper reviews the theoretical background for the use of progestins in advanced breast cancer and the clinical experience obtained from 13 major studies. The average rate of response is about 30%, with somewhat higher rates when the dominant site of disease is localized to soft tissue and to bones, compared with viscera. Furthermore it seems that cross resistance between progestin therapy and other endocrine therapies is only partial. However, response rates related to previous therapy and to important prognostic variables such as age of the patient, disease-free interval and hormone receptor content of the tumor tissue are poorly elucidated. Only limited data are available concerning response rate in relation to dose and route of administration and data from prospective randomized trials to analyze these relations are still lacking. Considering the only modest side effects of treatment with progestins and the clinical and theoretical evidence favoring a mode of action different from that of other endocrine therapies, progestins are drugs with interesting qualities. Therefore future controlled studies with progestins alone or in combination with other systemic therapies should be carried out to establish the therapeutic efficacy of progestin therapy in primary and advanced disease.

Age Factors↗

PubMed2005

Maternal progestin intake and risk of hypospadias.

BACKGROUND: Previous studies have suggested that maternal intake of progestins during early pregnancy may be associated with an increased risk of hypospadias. Progesterone and its derivatives are commonly prescribed during early pregnancy, for example, in cases of luteal phase dysfunction and in conjunction with ovulation stimulation drugs. OBJECTIVE: To examine whether risk of hypospadias was associated with periconceptional progestin intake. DESIGN AND SETTING: The National Birth Defects Prevention Study, a population-based, multistate, case-control study including deliveries that had estimated due dates from October, 1997 to December, 2000. PARTICIPANTS: Participation in the study was 71% among case mothers and 68% among control mothers. This analysis included 502 subjects diagnosed with second- or third-degree hypospadias (ie, the urethra opened at the penile shaft, scrotum, or perineum) and 1286 male, live-born, nonmalformed control subjects. RESULTS: Forty-two case mothers (8.4%) and 31 control mothers (2.4%) reported any pregnancy-related progestin intake from 4 weeks before through 14 weeks after conception, resulting in an odds ratio of 3.7 (95% confidence interval [CI], 2.3-6.0). Analyses stratified by several potential covariates also suggested elevated risks. For example, among the 10 cases and 13 controls who did not report any fertility-related procedures or treatments other than progestins, the odds ratio was 2.2 (95% CI, 1.0-5.0). Progestin intake for the purpose of contraception was not associated with increased risk. CONCLUSION: This study found that pregnancy-related intake of progestins was associated with increased hypospadias risk.

Abnormalities, Drug-Induced↗

PubMed1990

Autoradiographic localization of progestin-concentrating cells in the brain of the zebra finch.

The production of song in passerine birds is under the control of steroid hormones, and brain regions involved in song production have been shown to contain androgen and/or estrogen receptors. Studies to date, however, have not considered the possible role of progestins in this behavior. As one approach to this question, the autoradiographic method was used to investigate the distribution of progestin-concentrating cells in the brain of the adult male zebra finch (Poephila guttata) after injection of the radiolabeled synthetic progestin [17 alpha-methyl-3H]-promegestone. In the telencephalon, identifiable groups of progestin-accumulating cells were found in the hyperstriatum dorsale, at the medial edge of the lobus parolfactorius, and in the medial septum. In the diencephalon, labeled groups of cells were found in the preoptic area, through much of the medial hypothalamus--including nucleus periventricularis magnocellularis, nucleus medialis hypothalami posterialis, and area infundibularis--and in the medial spiriform nucleus and dorsomedial thalamus. In the myelencephalon, labeled cells are described at the dorsal edge of the medulla and scattered lateral to nXII. These findings offer no support for the hypothesis that progestin acts on any of the known song regions, but do suggest areas of progestin action in the avian central nervous system outside of the known song system. Not surprisingly, these include many areas of the medial hypothalamus and other midline structures.

Animals↗

PubMed1983

Cytosol and nuclear estrogen and progestin receptors and 17 beta-hydroxysteroid dehydrogenase activity in non-diseased tissue and in benign and malignant tumors of the human ovary.

Significant but low concentrations (mean 8 fmol/mg cytosol protein) of cytosol estrogen receptors were found in 57% of non-diseased ovarian tissues, and higher concentrations (mean 211) of cytosol progestin receptors in all these tissues. An approximately similar distribution was found for the presence of nuclear female sex steroid receptors; the mean concentrations were 159 and 1149 sites/cell, for estrogen and progestin receptors, respectively. There were no major differences in these parameters between pre- and postmenopausal non-diseased ovaries. The activities of ovarian 17 beta-hydroxysteroid dehydrogenase (17-HSD) did not display correlations between circulating progesterone concentrations in pre- or postmenopausal women with non-diseased ovaries. The majority of benign epithelial tumors contained significant concentrations of cytosol estrogen receptors, and all showed cytosol progestin receptors. The concentration of estrogen receptors was identical to that seen in non-diseased ovaries (mean 9 fmol/mg cytosol protein), whereas that of progestin receptor was significantly lower (mean 95). Nuclear female sex steroid receptors were measured in all benign tumors, and their concentrations were significantly higher than in normal ovaries (440 and 3218 sites/cell for estrogen and progestin receptors, respectively). No difference in 17-HSD activities were detected between normal ovaries and benign tumors. In malignant ovarian tumors, the picture was different from that found in normal ovarian tissues and benign tumors. Cytosol estrogen receptor was found in 89% of malignant epithelial tumors, and its concentration was significantly higher (mean 64 fmol/mg cytosol protein). Cytosol progestin receptor was found in 91%, and its concentration (mean 75) was significantly lower than in normal ovarian tissue or benign ovarian tumors. Nuclear female sex steroid receptor concentrations were intermediate between those seen in non-diseased ovaries an in benign tumors. 17-HSD activity was significantly lower than in other tissue categories studied. In the small group (16) of non-epithelial ovarian carcinomas cytosol estrogen receptors were not found, whereas the results of other measurements did not display any coherent picture. Breast and endometrial carcinoma metastatic to the ovary showed receptor patterns which were typical of the primary tumors. When the different clinical stages (I-IV) of malignant epithelial ovarian tumors were compared, 17-HSD activity was significantly higher in the least advanced clinical stage (I), whereas no significant differences were found in the other parameters measured.(ABSTRACT TRUNCATED AT 400 WORDS)

17-Hydroxysteroid Dehydrogenases↗

PubMed2000

Progestin effects on long-term growth, death, and Bcl-xL in breast cancer cells.

The effect of progestins on proliferation of breast cancer has been a controversial area. We have consistently reported progestin stimulation of proliferation in the progesterone receptor-rich human breast cancer cell line T47D. Other authors, under other conditions, have agreed that progestins stimulate, but for just one turn of the cell cycle. To our knowledge, this is the first in vitro report to show progestin stimulation of human breast cancer cell growth for multiple, probably unlimited, cell cycles, while control cells are dying. This is accompanied by progestin up-regulation of the antiapoptotic protein bcl-xL, no effect on the proapoptotic protein bax, and, surprisingly, diminution of the antiapoptotic protein bcl-2. Thus, progestins both serve as survival factors and stimulate proliferation, implying a possible similar role in breast cancer patients. The data support the notion that many patients may benefit more from combined antiprogestin-antiestrogen therapy than from antiestrogen alone, and suggest bcl-x(L) as a possible target for breast cancer therapy.

Apoptosis↗

PubMed1994

Recency, duration, and progestin content of oral contraceptives in relation to the incidence of endometrial cancer (Washington, USA).

Women who have used combined oral contraceptives (COC) have a reduced risk of endometrial cancer relative to that of women who have never used oral contraceptives, but it is unclear whether the size of the reduction is influenced by the progestin content of the preparation. We analyzed data from two population-based case-control studies of endometrial cancer to investigate this question. Among women aged 40 to 59 years who were residents of King or Pierce Counties, Washington (United States), incident cases who were diagnosed during 1975-77 or 1985-87 were identified. Personal interviews were conducted with 316 such women and their responses compared with those of 501 controls who were selected by household surveys or random-digit dialing. A reduced risk of endometrial cancer associated with COC use was present only among users of five or more years' duration, and even then only in women who were not long-term users of unopposed postmenopausal estrogens. Among these women, the relative risk (RR) of endometrial cancer did not differ according to the progestin potency of the COC used: it was equally low for women who had used a COC with low progestin content (RR = 0.2, 95 percent confidence interval [CI] = 0.1-0.8) as for women who had used a COC with high progestin content (RR = 0.3, CI = 0.1-0.9). Our results argue that, if the reduced risk of endometrial cancer in long-term users of COCs is due to the progestins contained in these preparations, that amount of progestin in most COCs exceeds the threshold amount needed to produce this beneficial effect.

Adult↗

PubMed2005

Estrogens, progestins, menopause and neurodegeneration: basic and clinical studies.

Two classes of ovarian steroids, estrogens and progestins, are potent in protecting neurons against acute toxic events as well as chronic neurodegeneration. Herein we review the evidence for neuroprotection by both classes of steroids, provide plausible mechanisms for these potent neuroprotective activities and indicate the need for further clinical trials of both estrogens and progestins in protection against acute and chronic conditions that cause neuronal death. Estrogens at concentrations ranging from physiological to pharmacological are neuroprotective in a variety of in vitro and in vivo models of cerebral ischemia and brain trauma as well as in reducing key neuropathologies of Alzheimer's disease. While the mechanisms of this potent neuroprotection are currently unresolved, a mitochondrial mechanism is involved. Progestins have been recently shown to activate many of the signaling pathways used by estrogens to neuroprotect, and progestins have been shown to protect against neuronal loss in vitro and in vivo in a variety of models of acute insult. Collectively, results of these animal and tissue culture models suggest that the loss of both estrogens and progestins at the menopause makes the brain more vulnerable to acute insults and chronic neurodegenerative diseases. Further clinical assessment of appropriate regimens of estrogens, progestins and their combination are supported by these data.

Animals↗

PubMed1985

Regulation of growth hormone and epidermal growth factor receptors by progestins in breast cancer cells.

A 24 hr incubation of T-47D human breast cancer cells with R5020, a synthetic progestin, resulted in a 200-250% increase in the specific binding of human growth hormone (hGH) and epidermal growth factor (EGF) by these cells. This effect was specific for progestins in that similar responses were observed with progesterone, medroxyprogesterone acetate and ORG 2058 but no significant increases in hGH or EGF binding were observed in cells incubated with testosterone, estradiol or hydrocortisone. Increased binding was due to an increase in the concentration of receptors (hGH, control = 6,490 +/- 500, progestin treated = 13,180 +/- 3,270 sites/cell; EGF, control = 33,380 +/- 7,410, progestin treated = 67,460 +/- 20,330 sites/cell) while the affinity constants for the hormone-receptor interactions were unchanged by progestin treatment. The specific binding of insulin, calcitonin, transferrin and concanavalin A was unaffected by these treatments. It is concluded that expression of hGH and EGF receptors in this breast cancer cell line is regulated by progestins.

Breast Neoplasms↗

PubMed1976

Changes in multiunit activity and EEG induced by the administration of natural progestins to flaxedil immobilized cats.

The effects of progesterone (P) and 7 of its metabolites on the EEG and multiunit activity (MUA) of various limbic structures were studied in flaxedil immobilized cats. Most progestins inhibited the MUA of the mesencephalic reticular formation, hippocampus and hypothalamus and induced cortical EEG synchronization. MUA changes in the mesencephalic reticular formation frequently preceded EEG synchronization. Progestins reduced in the 5 beta postition (pregnanolone, epipregnanolone and pregnanedion) inhibited neuronal discharge and synchronized EEG activity with shorter latencies and in lower doses than those reduced in the 5 alpha position (allopregnanolone and allopregnanedion). Progestins having the delta 4,3-keto structure (P, 20 alpha-hydroxy pregnenone, 20 beta-hydroxy pregnenone) induced electrophysiological changes with prolonged latencies and in doses significantly higher than ring A reduced progestins. Administration of epipregnanolone to "cerveau isole" preparations depressed neuronal firing in those structures located rostral to the level of the brain stem transection (hypothalamus, hippocampus), but failed to increase the already synchronized cortical activity. These results suggest that: a, ring A reduction increases the capacity of P and other delta 4,3-keto progestins to inhibit neuronal discharge in certain brain areas and b, changes in neuronal firing induced by progestins are not necessarily mediated through the cat brain stem reticular formation.

Animals↗