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B Parsons

Publications and source records attributed to B Parsons.

At least 55 records · Page 3Linked to original sources
PubMed1984

Organizational effects of testosterone via aromatization on feminine reproductive behavior and neural progestin receptors in rat brain.

The present studies were undertaken to determine whether estrogenic actions of testosterone during development govern the apparently irreversible suppression of feminine reproductive behavior in the male and lead to a suppression of the capacity of the ventromedial nucleus (VMN) of the hypothalamus to produce cytosol progestin receptors (CPRs) in response to estrogen priming. Timed-pregnant female rats received daily injections of the aromatase inhibitor 1,4,6-androstatriene-3,17-dione (ATD; 5 mg/0.2 ml) from the 14th day of pregnancy until parturition. Males exposed to ATD in utero received Silastic capsules containing ATD for the first 10 days of life. Some females from litters not exposed to ATD received injections of estradiol benzoate (EB; 10 micrograms) 6-12 h and 3 days after birth. The remaining pups not exposed to ATD served as controls. Pups were gonadectomized on days 60-70 and were tested for feminine reproductive behavior or killed for CPR measurements on days 85-90. To elicit behavior, animals received daily injections of EB (15 micrograms for 3 days) and one injection of progesterone (500 micrograms) 4 h before testing. To induce CPRs, animals received EB but not progesterone. Significantly less receptive and proceptive behavior was observed in males and females given perinatal EB than in normal females and males given perinatal ATD. The CPR content of the VMN in males was similar to that in females given perinatal EB and significantly less than that in normal females and males given perinatal ATD. Neonatal hormonal manipulation did not alter the CPR content of other hypothalamic or preoptic nuclei. These findings are consistent with the hypothesis that one event mediated by estradiol which underlies activation of feminine reproductive behavior is the induction of CPRs in the VMN. This capacity is apparently restricted by estrogen-mediated events in males during the perinatal period.

Androstatrienes↗
PubMed1983

Behavioral and neuroendocrine effects of long-term progesterone treatment in the rat.

Progesterone and estradiol, alone or in combination, were administered to ovariectomized rats for 2 weeks. Progesterone alone had no effect on body weight, luteinizing hormone (LH) secretion, receptivity or brain cytoplasmic progestin receptors (CPR). Progesterone in combination with estradiol significantly attenuated estrogen suppression of weight gain and estrogen stimulation of receptivity, the LH afternoon surge and induction of CPR, but did not affect the negative feedback of estrogen on morning LH levels. The decrease in CPR after 2 weeks of progesterone is very similar in magnitude to the decrease observed following acute treatment, suggesting that, unlike neurotransmitter agonists and glucocorticoids, progesterone does not cause down regulation of its receptors in the brain following chronic treatment.

Animals↗
PubMed1982

Characterization of estrogen stimuli sufficient to initiate cyclic luteinizing hormone release in acutely ovariectomized rats.

Estradiol (E)-filled Silastic capsules were implanted subcutaneously to characterize the estrogen stimulus sufficient to initiate cyclic LH secretion in female rats ovariectomized on diestrus 1 of the estrous cycle. Such capsules elevate preoptic area, hypothalamic and hypophysial cell nuclear estrogen receptor levels to proestrous values within 1/2 h following insertion; upon removal of the capsules, nuclear receptor levels decline monotonically to ovariectomized control levels by 8 h in brain and 12 h in pituitary. Three parameters of the E stimulus were studied: latent period, duration, and continuity. E stimuli, short in duration (7-12 h) and discontinuous in nature (3 h pulses 12 or 15 h apart), effectively stimulated LH surges on "proestrus'. However, these stimuli had to begin 30 h prior to the onset of LH release. Such a latent period for estrogen action was not observed when we monitored the ability of the same E stimuli to enhance pituitary responsiveness to GnRH. These studies demonstrate that the "rate-limiting step' for estrogen's positive feedback action is located within the estrogen-sensitive brain circuits controlling GnRH release and defines the temporal characteristics of E stimuli activating these circuits.

Animals↗
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↗
PubMed1982

Estradiol receptor levels in rat hypothalamic and limbic nuclei.

The amount of cytoplasmic receptor for the steroid hormone, estradiol (E2), was determined in 46 nuclei and subdivisions of rat brain. Individual nuclei were removed from 300-micrometers frozen sections according to the punch-out method of Palkovits (Palkovits, M. (1973) Brain Res. 59: 449-450), and the content of E2 receptor was measured with a sensitive radioligand binding method. Cytoplasmic receptors for E2 were distributed heterogeneously throughout the rat brain. The highest level of receptor (40 fmol/mg of protein) was found in the periventricular nucleus of the preoptic area, while low (1 fmol/mg) but detectable levels of receptors were found in such limbic regions as the nucleus of the diagonal band, the olfactory tubercle, and the cingulate cortex. Regions that were devoid of detectable receptor included the medial septum, the parietal cortex, and the ventral thalamus. Our results support the notion that E2 influences reproductive behavior and neuroendocrine function by binding to receptors in discrete areas of the brain and provide the first quantitative map of E2 receptors in individual rat brain nuclei.

Animals↗
PubMed1981

Sequential inhibition of progesterone: effects on sexual receptivity and associated changes in brain cytosol progestin binding in the female rat.

The purpose of this study was to examine the role of cytosol progestin receptors (CPRs) in the activation of mating behavior in the estrogen (E2) stimulated, ovariectomized rat, following the administration of a dose of progesterone (P; 2.5 mg) which is sufficiently large to inhibit the re-induction of sexual receptivity by subsequent P ('sequential inhibition'). In order to control for competition by unlabeled P in our binding studies, aliquots of cytosol supernatants were passed through LH-20 columns prior to in vitro incubation with the radioactive ligand, [3H]R5020 (double column assay). Three days following E2 priming, all animals used in behavioral studies received either P (2.5 mg) or vehicle injections (propylene glycol; PG) 24, 48 or 72 h prior to the administration of P (0.5 mg). When P (0.5 mg) was given 24 h after P or PG treatment, animals which had received P previously showed significantly decreased lordosis quotients (LQ), lordosis quality (LS) and proceptivity scores relative to PG controls ('sequential inhibition'). The inhibitory effects of previous P (2.5 mg) were transient, and were not observed if P (0.5 mg) was delayed until 72 h after P or PG treatment. Three days following E2 priming, all animals used in biochemical studies received either P (2.5 mg) or PG. When we did not control for competition by unlabeled P, [3H]R5020 binding in the cortex, mediobasal hypothalamus-preoptic area (MBH-POA) and pituitary was decreased by 60%, 3 h after 2.5 mg P. When we used the double column assay to remove P in the tissue, [3H]R5020 binding in all tissues was decreased by 20% at 3 h after 2.5 mg P. By 24 h, after 2.5 mg P, the competitive effect of tissue P on [3H]R5020 binding was not measureable; and cytosol progestin receptor (CPR) levels were less than or equal to those seen at 3 h. By 72 h after 2.5 mg P, CPRs had returned to control levels in all tissues. Our data suggest: (1) the double column assay is necessary to estimate CPR levels when P is present in the tissue; (2) when one controls for competition by P, CPR depletion 3 after P is measurable but not extensive; depletion occurs in tissues in which CPRs are induced by E2 (pituitary, MBH-POA), as well as in cerebral cortex, where CPR levels are not included by E2; (3) at 24 h, CPR levels are less than or equal to those seen at 3 h in all tissues; this may be the result of the initial depletion associated with nuclear translocation, or it may indicate that P regulates its own receptor concentration in the central nervous system (down-regulation); and (4) after a large dose of P (2.5 mg), reduced CPR levels are correlated with P's reduced ability to facilitate sexual receptivity.

Animals↗
PubMed1981

Temporal relationship between cell nuclear progestin receptor levels and sexual receptivity following intravenous progesterone administration.

This study was designed to assess the temporal relationship between the appearance and retention of cell nuclear progestin receptors in hypothalamus and the facilitation and decline of feminine sexual behavior following an i.v. injection of progesterone (P). Nuclear translocation of progestin receptors preceded the earliest appearance of behavior. The behavioral effects of P outlasted the nuclear progestin receptor elevation by several hours. Our results are consistent with the idea that P-induced effects on feminine sexual behavior involve genomic activation.

Animals↗
PubMed1981

Protamine sulphate hypersensitivity.

Protamine hypersensitivity has been documented by intra-dermal skin testing in three patients who demonstrated sudden cardiovascular collapse and bronchospasm following the use of intravenous protamine sulphate. All patients had been given protamine previously. The effects of the anaphylactic response were terminated quickly by the administration of intravenous adrenaline associated with plasma volume expansion. Intra-dermal skin testing against all anaesthetic agents is recommended so that the specific allergen can be identified. In patients who are shown to be allergic to protamine sulphate and who require cardiac or vascular surgery careful monitoring of heparin dosage and neutralisation with hexadimethrine (Polybrene) intravenously appears to be a safe alternative.

Anaphylaxis↗