bluuebunny/crossref_metadata_2025_split huggingface dataset:
Random and Non‐Random Coincidence Between Luteinizing Hormone Peaks and Follicle‐Stimulating Hormone, Alpha Subunit, Prolactin and Gonadotropin‐Releasing Hormone ulsations
Authors: Veldhuis Johannes D. , Iranmanesh Ali , Clarke Lain , Kaiser Donald L. , Johnson Michael L. 
Published: September 2006

AbstractWe have examined the co‐pulsatility of luteinizing hormone (LH) and prolactin, LH and follicle‐stimulating hormone (FSH), and LH and α subunit in normal men. We tested whether the degree of physiologically observed co‐pulsatility (peak coincidence) significantly exceeded expected random concordance between independently pulsating hormone series. To this end, computer simulations were used to create synthetic endocrine time series pulsating randomly and independently at known frequencies. Resultant predictions of the mean, variance and probability distribution of the number of randomly coincident peaks permitted us to test the null hypothesis that physiologically observed hormone co‐pulsatility was due to chance peak associations alone. Physiological observations were made in 33 normal men and in six ovariectomized ewes subjected to combined hypothalamo‐pituitary and jugular venous catheterization. The following salient results were obtained: 1) random peak coincidence rates between independently pulsating hormone series were substantial at high pulse frequencies, but such random rates were significantly exceeded in the case of gonadotropin‐releasing hormone and LH peaks (P< 0.0001); 2) random coincidence was further increased when coincidence was defined as peak maxima occurring not only simultaneously but also within some defined time window (e.g. ±10 min, as commonly done in the literature); 3) significant co‐pulsatility could be demonstrated for simultaneous LH and FSH pulsations in normal men (P< 0.0001); 4) coincidence rates for 10‐min lagged (but not for simultaneous) LH and prolactin pulses were significantly more likely than chance associations; 5) observed coincidence between LH and a subunit pulses significantly exceeded expected (random) peak overlap (P<0.001); and 6) in contrast, hormone peaks in different men were only randomly associated.We conclude that based upon the means, variances and probability distributions calculated here, available reports on peak coincidence between pulsatile neuroendocrine time series must be re‐examined in the light of high rates of random coincidence observed between independently pulsating hormone series.
Multifaceted Interaction of Corticosteroids with the Intracellular Receptors and with Membrane GABAA Receptor Complex in the Rat Brain
Authors: Sutanto Win , Handelmann Gail , de Bree Freddy , de Kloet E. Ronald 
Published: September 2006

Abstract In vitro assays using crude synaptosomal membrane preparations from the cortex and cytosolic fraction of hippocampus have shown that in the brain, steroids can bind to the intracellular corticosteroid receptors as well as to the membrane‐bound GABA‐receptor complex. Corticosteroid, deoxycorticosterone and spironolactone bound with higher affinity to the mineralocorticoid (relative binding affinity (IC50 in nM) 1.2, 3.9 and 4.9, respectively) than to the glucocorticoid receptors (IC50 5.2, 14.0 and 88.0 nM, respectively) in hippocampal cytosol. They enhanced significantly the binding of [35S]t‐butylbicyclophosphorothionate to cortical membrane. Steroids such as 3α,5α‐tetrahydroxydeoxycorticosterone and 3a‐hydroxy‐5α‐dihydroprogesterone displaced the binding of [35S]t‐butylbicyclophosphorothionate with IC50 (in nM) of 236.7 and 315.0, respectively. In the presence of 10 to 12.5μM added GABA, they bound with higher affinity (IC50 18.0 and 20.5 nM, respectively). Pentobarbital also bound to this site with IC50 of 430,000 and 240,000 nM, respectively, in the absence and presence of GABA. These compounds also enhanced the binding of [3H]flunitrazepam which was not affected by the presence of added GABA. They showed no affinity for mineralocorticoid or glucocorticoid receptors.Data from this study showed that steroids which preferentially bound to the mineralocorticoid receptor sites (corticosterone, deoxycorticosterone and spironolactone) also enhanced the binding of [35S]t‐butylbicyclophosphorothionate to their recognition sites. Steroids which did not interact with the intracellular receptors (3α,5α‐tetrahydroxydeoxycorticosterone and 3a‐hydroxy‐5α‐dihydroprogesterone) displaced [35S]t‐butylbicyclophosphorothionate binding and enhanced [3H]flunitrazepam binding.
Medial Preoptic Microimplants of the Antiestrogen, Keoxifene, Affect Luteinizing Hormone‐Releasing Hormone mRNA Levels, Median Eminence Luteinizing Hormone‐Releasing Hormone Concentrations and Luteinizing Hormone Release in Ovariectomized, Estrogen‐Treated Rats
Authors: Petersen Sandra L. , Cheuk Chad , Hartman Richard D. , Barraclough Charles A. 
Published: September 2006

AbstractWe examined the temporal changes in plasma luteinizing hormone (LH) levels, median eminence luteinizing hormone‐releasing hormone (LHRH) concentrations and LHRH mRNA levels in estrogen‐treated, ovariectomized rats with empty or antiestrogen‐ containing microcannulae stereotaxically implanted into the medial preoptic area. Neither treatment disrupted the negative feedback effects of estrogen on LH secretion, but antiestrogen (Keoxifene) blocked the afternoon LH surges. In rats exhibiting LH surges, median eminence LHRH concentrations were similar at 0800, 1200 and 1600 h, but they were significantly elevated by 2000 h. In contrast, no alterations in LHRH concentrations occurred in the Keoxifene‐treated group. LHRH mRNA levels in control rats were significantly elevated at 1200, 1600 and 2000 h compared with 0800 h, but LHRH mRNA levels in Keoxifene‐treated rats did not change significantly over the time period examined. When we compared treatment effects over time we saw that serum LH levels were significantly higher in control than Keoxifene‐treated rats only at 1600 and 2000 h. Median eminence LHRH concentrations did not differ between treatment groups until 2000 h when control animals had significantly higher levels than those of Keoxifene‐treated animals. LHRH mRNA levels in Keoxifene‐treated rats were significantly higher than those of controls at 0800 hand significantly lower at 1600 h. No differences in LHRH mRNA levels were detected between groups at either 1200 h or 2000 h. In summary, although it was not clear on which neuronal system estrogen acted, depriving medial preoptic neurons of this steroid in systemically estrogenized rats certainly disrupted the neural mechanisms involved in surge, but not basal LH release. In addition, neither LHRH mRNA levels nor median eminence LHRH concentrations showed variations within the period studied when the estrogen‐sensitive mechanisms involved in LH release were disrupted. Therefore, the changes in LHRH mRNA levels and LHRH concentrations in the median eminence seen in surging animals probably resulted from the same neural events which triggered LH release.
The Brain Renin‐Angiotensin System and the Regulation of Prolactin Secretion in Female Rats: Influence of Ovarian Hormones
Authors: Myers Lin S. , Steele Marianne K. 
Published: September 2006

AbstractThis study was designed to investigate the effects of exogenous and endogenous angiotensin II (All) on prolactin release in ovariectomized rats, with and without estrogen and progesterone pretreatment. In the first series of experiments, All or vehicle was injected into the third cerebral ventricle of conscious, freely‐moving rats. In both treated and untreated rats, administration of 50 ng All suppressed prolactin levels within 15min of injection, compared to vehicle‐injected rats. In untreated rats, prolactin levels returned to baseline values by 30 min, while in treated rats, prolactin levels remained suppressed for an hour.In the second series of experiments, the involvement of endogenous brain All in tonically suppressing prolactin release was assessed by administering either All receptor blockers (saralasin or sarthran) or an All synthesis inhibitor (enalaprilat, an inhibitor of the conversion of angiotensin I to All). Neither All receptor blockade nor converting enzyme inhibition resulted in any change in prolactin levels in untreated levels in untreated rats. However, following treatment with ovarian steroids, infusion of saralasin or injection of enalaprilat resulted in a significant increase in plasma prolactin tilers. During saralasin infusion, prolactin levels were significantly increased by 15 min and continued to be higher than controls at 60 min. After enalaprilat administration, prolactin levels did not rise significantly until 90 min and then remained elevated up to 120 min post‐injection. These latter results suggest that at least one h is required for maximal inhibition of angiotensin synthesis in the brain.These data demonstrate that low doses of All suppressed basal prolactin secretion in both untreated and ovarian steroid‐treated, ovariectomized rats. However, treated rats appeared to be more sensitive than untreated animals to the prolactin‐lowering effects of centrally administered All. The lack of prolactin response in untreated rats when brain All synthesis was inhibited or All receptors were blocked suggests that, in the absence of ovarian steroids, endogenous All was not acting tonically to suppress prolactin secretion. Following exposure to ovarian steroids, however, the endogenous brain All system appeared to be activated and involved in controlling prolactin release.
Effects of Neonatal Exposure to Estradiol on Prolactin Secretion and Activity of the Tubero‐lnfundibular Dopamine System in Young Adulthood: Comparison with Neonatal Prolactin Deficiency*
Authors: Crowley William R. , Shah Girish V. , Watanobe Hajime , Grosvenor Clark E. 
Published: September 2006

AbstractPrevious results from this laboratory indicate that female rats who consume milk deficient in prolactin (PRL) during the neonatal period subsequently display hyperprolactinemia, associated with decreased activity in the tubero‐infundibular dopamine (DA) system and decreased lactotrope responsiveness to DA receptor stimulation. The present studies tested whether these neuroendocrine consequences of neonatal PRL deficiency can be mimicked by exposure of neonatal rats to estradiol. Female rats were injected sc with 1 mUg estradiol benzoate or oil vehicle on postpartum Days one to 3, while in other experiments, females were made neonatally deficient in PRL through treatment of their mothers with the DA agonist bromocriptine, a treatment that reduces the levels of PRL in milk. Females treated neonatally with estradiol benzoate, as well as offspring of the bromocriptine‐treated mothers, displayed hyperprolactinemia as young adults, as compared to their respective vehicle‐matched controls, and in both cases, this was abolished by ovariectomy, indicating dependence upon ovarian secretions. As reported previously in neonatal PRL‐deficient females, neonatal estradiol benzoate‐treated animals also exhibited reduced steady state levels and decreased turnover rates of DA in the median eminence when 35 days of age. DA levels and turnover rates in this region were still significantly reduced on postpartum Day 60. The DA agonist bromocriptine suppressed PRL release to a similar extent in cultured anterior pituitary cells from neonatal estrogen‐treated and control rats, suggesting normal responsiveness of DA receptors on lactotrope cells in both groups. The present results confirm the ability of estradiol treatment or induction of a PRL deficiency during the early neonatal period to induce subsequent hyperprolactinemia in female rats, and further indicate that the hyperprolactinemic conditions resulting from either neonatal manipulation are dependent on the ovary and are associated with decreased levels and turnover of DA in the median eminence during the prepubertal period. Although these findings suggest that increased exposure to estradiol during the neonatal period may underlie the similar effects of neonatal PRL deficiency, the further observations in neonatal estrogen‐treated rats that 1) decreased DA turnover in the median eminence persists at Day 60, and 2) lactotrope responsiveness to DA is normal, differ from results obtained previously in PRL‐deficient rats. Thus, enhanced exposure to estrogen during the neonatal period does not appear to account for all of the neuroendocrine consequences of neonatal PRL deficiency.
Direct Stimulation of Growth Hormone Secretion by Galanin in the Domestic Fowl*
Authors: Cheung A. , Hall T. R. 
Published: September 2006

AbstractGalanin, a novel peptide originally isolated from porcine intestine, has a wide distribution in the nervous system and is known to enhance the release of growth hormone in mammals, though the mechanism of its actions is still subject to debate. In the current study, the effects of galanin on growth hormone secretion in the domestic fowl were investigated. Intravenous injections of galanin into both 8‐week old and 18‐week old female Hubbard broilers produced marked increases in plasma growth hormone, similar in magnitude to that evoked by human growth hormone‐releasing factor. Galanin produced dose‐related increases in growth hormone release, with a peak response occurring within 10 min of administration. Growth hormone release in response to a maximal challenge of growth hormone‐releasing factor was further augmented when galanin was given at the same time. Galanin stimulated growth hormone release from chick hemipituitary glands in vitro, a response which was not dependent upon hypothalamic input. In addition, galanin potentiated the actions of growth hormone‐releasing factor on growth hormone release in vitro and these responses were reversed by somatostatin. These results show that galanin is able to stimulate growth hormone release in the domestic fowl by acting directly on the pituitary gland.
Atrial Natriuretic Peptide Secretion from Fetal Rat Diencephalon in Culture
Authors: Levin Ellis R. , Loughlin Sandra E. , Kaplan Gary 
Published: September 2006

AbstractThe presence of a distinct brain pool of the atrial natriuretic peptides (ANP) has been established. To determine the molecular forms and regulation of secretion of ANP, we studied fetal rat diencephalic neurons and glia in primary culture. ANP immunoreactivity determined by radioimmunoassay was found only in the neuron predominant cultures. The neurons contained mainly ANP (103–126) and less ANP (102–126), but secreted only ANP (103–126) into the medium after potassium and glutamate‐dependent depolarization. Little, if any, ANP (99–126), the predominant form which circulates in plasma and originates from the heart, was secreted. The ability of potassium and glutamate to cause a mean 50% increase of ANP secretion above baseline was abolished after deleting calcium chloride from the medium. In contrast, hypo‐ or hyperosmolarity or increased sodium content in the incubation medium did not influence ANP secretion. These studies indicate that regulative secretion of ANP occurs from primary cultures of predominantly diencephalic neurons, probably accounting for the high concentrations of these peptides in this area of the brain. The forms of ANP contained within the cells and secreted after depolarization are different from ANP secreted from neonatal rat atrial myocytes. In contrast to myocytes, varying sodium or osmolarity did not cause ANP secretion. We postulate that influences on ANP production/secretion in the brain may be distinct from the heart.
Relationship of Gonadal Hormone Administration, Sex, Reproductive Status and Age to Monoamine Oxidase Activity Within the Hypothalamus
Authors: Luine Victoria , Hearns Michelle 
Published: September 2006

AbstractActivity of Type A monoamine oxidase (MAO) was measured in microdissected samples from preoptic‐hypothalamic and hindbrain areas of young male and female rats, and aged female rats. Administration of estradiol and progesterone, in doses sufficient to facilitate lordosis behavior and induce a luteinizing hormone surge in ovariectomized, but not castrated rats, was associated with sexually dimorphic changes of MAO activity within the hypothalamus. Forty‐two h following estradiol benzoate administration, increased MAO activity was measured in the ventromedial nucleus (VML) and midbrain central gray of females, while decreased MAO activity was measured in the VML and arcuate‐median eminence (ArME) of males. Progesterone administration to estradiol benzoate‐primed rats was associated with decreased MAO activity in the VML and medial preoptic nucleus (mPOA) of females and decreased activity in the dorsal raphe nucleus of males. Activity of MAO on diestrus, proestrus and estrus was assessed in ten preoptic‐hypothalamic and hindbrain sites. Differences between days of the cycle were limited to the mPOA, ArME and VML. While activities were generally lowest at estrus, these areas exhibited different patterns of activity across the cycle. Activity was highest at proestrus in the mPOA and highest at diestrus in the VML and ArME. Activity of MAO in some areas of 25‐month old, diestrus rats was altered as compared to young, cycling rats; however, ageing was not associated with widespread changes in MAO activity. In the suprachiasmatic nucleus, aged rats showed approximately 30% less activity than young rats. In the mPOA, VML and ArME, activity in aged females was different from some, but not all, days of the estrous cycle. These results show that MAO activity changes within specific hypothalamic sites when the neuroendocrine axis is altered. Since the changes are present in areas where activity of rnonoaminergic systems is critical for initiating gonadotrophin surges and inducing lordosis behavior, these results provide initial evidence that catabolism of monoamines by MAO may contribute to rnonoaminergic regulation of reproductive function.
Effect of Naloxone on the Secretion of Corticosterone Induced by Gamma‐Hydroxybutyric Acid in Male Rats
Authors: Miguez M. I. , Aldegunde M. 
Published: September 2006

AbstractThe effect of intraperitoneally administered γ‐hydroxybutyrate on the hypothalamo‐hypophysial‐adrenocortical axis was studied. A significant increase in plasma corticosterone was induced by the administration of γ‐hydroxybutyrate (100 mg/kg). The lack of antagonism of this action of γ‐hydroxybutyrate by picrotoxin or bicuculline pretreatments (GABAergic antagonists), suggests independence from the GABAergic system. Neither dopaminergic nor serotoninergic systems intervened in the γ‐hydroxybutyrate‐stimulating effect on the hypothalamo‐hypophysial‐adrenocortical axis. Both corticosterone release and synthesis in adrenocortical cells was not significantly affected by γ‐hydroxybutyrate, suggesting that this is possibly due to a central action of γ‐hydroxybutyrate. The increase in corticosterone levels was probably mediated by an opioid receptor, since a strong similarity existed between the effects of γ‐hydroxybutyrate and those of morphine. Moreover, the results show that the opioid‐receptor involvement was demonstrated by the naloxone‐sensitivity of the γ‐hydroxybutyrate effects.
Secretion of GAWK, a Presumed Product of Chromogranin B Processing, by a Human Medullary Thyroid Carcinoma Cell Line: Effect of Phorbol Ester, Forskolin and Calcium‐lonophore
Authors: Iguchi H. , Kameya T. , Kadoya K. , Shimaoka K. 
Published: September 2006

AbstractGAWK was isolated from human pituitary glands and presumed to be a processing product of human Chromogranin B. In the present studies, we investigated effects of phorbol ester (TPA), forskolin and Ca2+‐ionophore (A23187) on GAWK secretion using a human medullary thyroid carcinoma‐derived cell line (TT‐cell). A dose‐responsive stimulation of GAWK‐like immunoreactivity (LI) secretion was found in the presence of TPA as well as forskolin. A23187 caused an increase of GAWK‐LI secretion and addition of TPA together with A23187 revealed an additive effect on the GAWK‐LI secretion. These findings indicate that GAWK‐LI is a secretory peptide in the TT‐cells and suggest that A and C kinase, and possibly Ca2+‐calmodulin transduction systems are involved in the GAWK‐LI secretion by the TT‐cells. TT‐cells may provide a good model for the investigation of regulation of Chromogranin secretion.
Expression of Histamine H1‐Receptors in Xenopus Oocytes Injected with Messenger Ribonucleic Acid from Bovine Adrenal Medulla: Pertussis Toxin Insensitive Activation of Membrane Chloride Currents
Authors: Meyerhof Wolfgang , Schwärzt Jürgen R. , Höllt Volker , Richter Dietmar 
Published: September 2006

AbstractHistamine H2‐receptors have been identified in Xenopus oocytes previously microinjected with poly(A) + ribonucleic acid from bovine adrenal glands. Bath application of histamine to ribonucleic acid‐primed oocytes evoked concentration‐dependent, oscillating membrane currents under voltage‐clamp conditions. H1‐receptor specific antagonists clemastine, doxepin, pyrilamine, promethacine, diphenylhydramine, dephenylpyraline and chlorpheniramine, but not H2‐receptor antagonists, cimetidine and ranitidine, inhibited histamine‐induced responses. Membrane currents evoked by bath‐applied histamine were insensitive to pertussis toxin, carried by chloride ions and dependent on intracellular but not extracellular calcium.
Arginine Vasopressin‐Anti‐Idiotypic Immunostaining of Human Brain Cells
Authors: Joseph S. A. , Pilcher W. H. , Knigge K. M. , Abood L G. , Michael G. J. 
Published: September 2006

AbstractPolyclonal anti‐idiotypic antibodies, generated against the IgG fraction of antisera to arginine vasopressin (AVP), were shown to recognize two proteins in rat brain and bovine pituitary associated with [3 H]AVP binding. Immunochemical analyses with these antisera revealed reactivity in paraventricular and supraoptic nucleus neuronal elements and in terminals of the posterior pituitary in the human central nervous system. With the use of a dual immunocytochemical staining technique employing both the anti‐idiotype and idiotype for AVP it was possible to demonstrate a pattern of AVP‐anti‐idiotypic‐immunoreactivity on AVP neuronal elements which suggests the existence of autoreceptors.