bluuebunny/crossref_metadata_2025_split huggingface dataset:
In vitro Effects of 17Beta‐Estradiol on Thyrotropin‐Releasing Hormone‐Induced and Dopamine‐lnhibited Prolactin Release from Adult Male Rat Lactotrophs in Primary Culture
Authors: Zhang Jin , Chen Chen , Kukstas Lucy Anna , Verrier Dany , Vincent Jean‐Didier , Israel Jean Marc 
Published: September 2006

AbstractContinuous cell perifusion and reverse hemolytic plaque assay have been used to show a regulatory action of 17 β‐estradiol on lactotroph responsiveness to thyrotropin‐releasing hormone (TRH) or dopamine (DA) in vitro. Lactotroph‐enriched cell cultures were obtained from adult male rats after trypsinization and mechanical dissociation followed by separation on a continuous bovine serum albumin gradient at unit gravity. After 7 days in culture, perifusion experiments showed that prolactin was continuously released and this release was increased by TRH and decreased by DA. Both TRH‐induced secretion and DA‐induced inhibition of prolactin release were dose‐dependent with a half maximal effect obtained at 7 × 10−9 M for TRH and at 10−9 M for DA. It was shown by reverse hemolytic plaque assay that about 55% of the cells were plaque‐forming (lysis of red blood cells) and were thus identified as prolactin‐secreting cells. This was similar to a previous result obtained by immunofluorescent staining. Heterogeneity among lactotrophs with regard to the quantity of prolactin released was clearly shown by the varying plaque areas in all preparations. In order to make a quantitative analysis of the effect of 17 β‐estradiol on TRH‐stimulation and DAergic inhibition in these heterogeneous prolactin cells, they were divided into two groups: large plaques (≥ 3 × 103μ m2) constituted about 35% of all plaque‐forming cells, and small plaques (< 3 × 103μ m2), about 65%. Pretreatment with 17β‐estradiol (10−8 M) either for 10 h or 48 h markedly increased TRH‐stimulated prolactin release and decreased the inhibitory effect of DA both in perifusion and reverse hemolytic plaque assay experiments. However, these pretreatments did not change the values of half maximum dose for TRH and DA. TRH transformed about 7% of the small plaques into large plaques and this proportion was increased to 25% after 17β‐estradiol treatment. On the contrary, DA and its more stable analogue bromocriptine increased the percentage of small plaques by 10% to 15% but this effect was decreased after 17β‐estradiol treatment. We conclude that: 1) Normal rat pituitary lactotrophs show heterogeneity with respect to their spontaneous release and responsiveness to TRH and DA; 2) pretreatment with 17β‐estradiol increases the response to TRH and decreases the response to DA without altering the doses at which they have half maximal effect; 3) there is no significant difference between the effect of 17β‐estradiol obtained after 10 h and after 48 h pretreatment.
Immunocytochemical Localization of Angiotensinogen and Angiotensin II in the Rat Pituitary
Authors: Thomas Walter G. , Sernia Conrad 
Published: September 2006

AbstractThe presence and distribution of angiotensinogen and angiotensin II (All) were demonstrated in rat pituitary by immunocytochemical staining with the avidin‐biotin‐peroxidase method, using primary polyclonal antibodies specific for angiotensinogen and All. Silver enhancement of the reaction product was used to intensify lightly stained areas. Attempts were made to identify immunopositive cells by colocalization studies with antisera against luteinizing hormone, prolactin and S‐100, a glial cell protein. In the anterior pituitary, angiotensinogen‐immunoreactivity was observed in cells lining follicle‐like structures. These cells, which were irregularly shaped and had processes extending between the glandular cells, did not colocalize with any of the reference antisera and are therefore of unknown cell type. The follicular endothelium was also immunopositive for angiotensinogen. After silver intensification, dispersed immunoreactive glandular cells were consistently observed in the anterior lobe. A proportion of these costained for luteinizing hormone, but not prolactin or S‐100, indicating their identity as gonadotrophs. In the posterior pituitary, angiotensinogen immunostaining was associated only with the vasculature, while groups of immunopositive cells were observed in the medial region of the intermediate lobe after silver enhancement. All‐immunoreactivity was observed in large cells preferentially located at the poles of the anterior pituitary which also costained for luteinizing hormone. No staining was observed in either the posterior or intermediate lobes. The presence of immunoreactive angiotensinogen in all three lobes of the pituitary suggests that there are sites, in addition to gonadotrophs, at which the intracellular production of All could occur.
Activation of Hypothalamic Gamma‐Aminobutyric Acid Receptors Resets the Pendulum of the Growth Hormone Clock
Authors: Willoughby J. O. , Kapoor R. 
Published: September 2006

AbstractPlasma levels of growth hormone in male rats exhibit an ultradian rhythm having a periodicity of 3 to 4 h, bursts of growth hormone being separated by troughs when growth hormone secretion ceases. To determine if neurons in the vicinity of somatostatin neurons in the preoptic/anterior hypothalamic area participate in the generation of the rhythm, we temporarily inhibited this region with injections of the γ‐aminobutyric acid agonist, muscimol, in unanaesthetized rats previously prepared with a venous catheter and stereotaxically implanted intracerebral guide tubes. The injection resulted in an immediate burst of growth hormone release, followed by a trough period and another growth hormone burst, 3.4 ± 0.1 h later. The induction of a trough and synchronization of growth hormone bursts was not reproduced by a burst of intravenously injected exogenous growth hormone at least as large as the first burst initiated by muscimol. These findings indicate that, in the short term, the ultradian rhythm is independent of growth hormone feedback and provide the first evidence that structures in the anterior hypothalamus receiving a γ‐aminobutyric acid input are an important component of the neural generator of the ultradian rhythm of growth hormone.
Diverse Effects of Norepinephrine on Vasopressin Release may Reflect Modulation by Hypotonicity
Authors: Sladek Celia D. , Yagil Ghana 
Published: September 2006

AbstractPrevious studies in this laboratory and others have demonstrated both stimulation and inhibition of vasopressin release by norepinephrine. In other regions of the central nervous system, diverse effects of norepinephrine reflect activation of different types of adrenergic receptors and the interaction of norepinephrine with other regulatory signals. In this study, the role of these two mechanisms in the diverse action of norepinephrine on vasopressin release were examined using organ‐cultured explants of the hypothalamo‐neurohypophyseal system. Receptor‐specific adrenergic agonists were found to have different effects on vasopressin release, and their effects were dependent upon whether they were delivered in isotonic saline or distilled water. When delivered in isotonic saline at a concentration of 10−5 M, norepinephrine and phenylephrine, an α1‐adrenergic agonist, increased vasopressin release (P< 0.005 and P< 0.025, respectively); isoproterenol (10−5 M), a β‐adrenergic agonist, did not alter vasopressin release; and clonidine, an α2‐adrenergic agonist, was ineffective at 10−5 M, but stimulated vasopressin release at 10−4 M (P<0.024). However, when these agonists were delivered in 10 μl of distilled water, their effects on vasopressin release were different. This amount of distilled water lowered the osmolality of the culture medium by 3 to 5 mosmol/kg H2O, but did not significantly alter vasopressin release. Vasopressin release was reduced below basal levels when norepinephrine (10−5 M) or clonidine (10−6 M) were delivered in distilled water (P<0.025), but it was not significantly different from basal when phenylephrine or isoproterenol (10−5 M) were delivered in distilled water. These data support the hypothesis that osmotic signals modulate the effect of norepinephrine on vasopressin release, and suggest that, at least in part, this reflects modulation of the type of adrenergic receptor dominating the regulation of vasopressin release.
Positive Feedback of Vasopressin on its Own Release in the Central Nervous System: in vitro Studies
Authors: Ramirez V. D. , Ramirez A. D. , Rodriguez F. , Vincent J. D. 
Published: September 2006

AbstractIn this paper evidence is shown that synthetic arginine vasopressin (AVP) can evoke marked in vitro release of endogenous immunoreactive AVP (I‐AVP) from male rat septal and hypothalamic tissue superfused in vitro. The stimulatory action was dosedependent with a maximal amplification factor of 2.3 when using 14 pg of synthetic AVP as the stimulus. It was highly specific since only AVP was effective and not three closely related substances such as lysine vasopressin, oxytocin and a 4–9 C fragment of AVP. This reproducible effect of AVP required, however, effective concentrations of bacitracin (10−4 to 10−5 M) in the superfusion medium to inhibit aminopeptidase(s) capable of inactivating AVP. Lastly, the stimulatory action of AVP on its own release was not blocked by a V1‐receptor antagonist of AVP but was blocked by a V2‐antagonist. It is proposed that this novel and robust positive feedback of AVP on its own release may be involved in the mechanism of memory consolidation of certain behavioral tasks known to be affected by AVP.
Central Nervous System Sites of Action of an Enkephalin Analogue, (D‐Met2, Pro5)‐Enkephalinamide, and Naloxone on the Secretion of Five Anterior Pituitary Hormones of Male Rats
Authors: Molnár Judith , Marton Jenõ , Halász Béla 
Published: September 2006

AbstractCentral nervous system sites of action of opioid peptides on pituitary hormone secretion were investigated. One nmol of an enkephalin analogue, (D‐Met2, Pro5)‐enkephalinamide, and 10 nmol of the opiate antagonist naloxone were injected into ten different regions of the brain of conscious male rats and their effect on the release of five anterior pituitary hormones tested. The injections were made through a special injection cannula which was inserted into the brain through a guide cannula fixed on the skull and implanted into the brain 5 to 7 days earlier. Both compounds injected into the medial septum, medial preoptic area and hypothalamic paraventricular nucleus affected prolactin, growth hormone and luteinizing hormone (LH) secretion. The enkephalin analogue stimulated prolactin and growth hormone and inhibited LH release. Naloxone induced the opposite effect. Drugs given into the hypothalamic ventromedial nucleus caused changes in plasma prolactin and growth hormone levels. Enkephalinamide increased and naloxone decreased plasma concentrations of both hormones. Administration of the compounds into the dorsal raphe area resulted in alterations of prolactin and LH release, the analogue caused elevation of prolactin and inhibition of LH release, whereas the opiate antagonist resulted in opposite changes. Only an LH response was obtained from the hypothalamic dorsomedial nucleus and a growth hormone response from the central amygdala. Also in these cases the enkephalin analogue decreased LH and elevated growth hormone plasma levels, and naloxone brought about a rise in LH and a diminution of growth hormone concentration. None of the regions were effective in inducing a clear‐cut adrenocorticotrophin or follicle‐stimulating hormone response. The parietal cortex, medial amygdala and the dentate gyrus were entirely ineffective sites. The findings suggest that in the brain there are multiple sites of action of opioids on pituitary trophic hormone secretion and the effective sites are not identical in terms of pituitary hormone response.
Inhibitory Effect of Progesterone on Occupied Estrogen Receptors of Anterior Pituitary and Uterus in Adult Rats
Authors: Fuentes Miguel A. , Muldoon Thomas G. , Mahesh Virendra B. 
Published: September 2006

AbstractThe acute effects of a single progesterone injection on estradiol receptor (E2R) binding in the anterior pituitary and uterus were examined in the mature ovariectomized rat. Adult ovariectomized female rats receiving estradiol were injected with various doses of progesterone followed 1 h later by a final injection of 2 μg of estradiol. All animals were sacrificed 1 h after estradiol and the E2R binding in the nuclei and cytosol was determined. In the anterior pituitary, progesterone decreased total nuclear E2R in a biphasic inhibitory pattern, with maximal effects at 0.8 and 4 mg/kg body wt doses of progesterone and a smaller decrease with the 2 mg/kg body wt dose. This progesterone‐induced decrease of nuclear E2R was due to a decrease in the occupied form of nuclear E2R. The unoccupied nuclear E2R and cytosol E2R binding were not altered by progesterone administration. In the uterus, progesterone caused a dose‐dependent decrease in total nuclear E2R binding. This effect also occurred in the occupied form of E2R. The uterine unoccupied nuclear E2R and cytosol E2R were not altered by progesterone administration.These studies emphasize differences in the tissue specificity of progesterone action on occupied nuclear E2R which are presumably responsible for the mediation of estradiol action, and provide a biochemical basis for our previous observations of multiphasic effect of progesterone on gonadotropin secretion.
Effects of Timed Melatonin Infusions and Lesions of the Suprachiasmatic Nuclei on Prolactin and Progesterone Secretions in Pregnant or Pseudopregnant Mink (Mustela vison)
Authors: Bonnefond C. , Martinet L. , Monnerie R. 
Published: September 2006

AbstractTo test the hypothesis that the duration of melatonin secretion may be a critical parameter in the transduction of photoperiodic signals on prolactin and progesterone secretions, timed intravenous melatonin infusions were carried out in intact and ganglionectomized pregnant and pseudopregnant mink. To localize the target sites of melatonin, electrolytic lesions of hypothalamic nuclei were performed in females receiving melatonin infusions. As a control, the first experiment was designed to confirm that pineal denervation by bilateral ablation of the superior cervical ganglion rendered the pregnant mink totally unresponsive to the inhibitory effects of short days on progesterone secretion. In the following experiments, timed intravenous melatonin infusions were carried out in intact and ganglionectomized females from Day 12 to 32 of pregnancy or pseudopregnancy. Daily infusions of melatonin for 16 h in intact females or for 11 or 13 h in ganglionectomized females suppressed the rise in plasma prolactin and progesterone levels. In intact as in ganglionectomized females, daily infusions of melatonin for 9 h delayed the rise in plasma prolactin concentrations without affecting the secretion of progesterone. In ganglionectomized females, saline infusions for 13 h or melatonin infusions for 7h did not modify the secretions of prolactin and progesterone. In ganglionectomized females bearing lesions of the Suprachiasmatic nuclei or the retrochiasmatic area, melatonin infusions for 13 h were still able to inhibit prolactin and progesterone secretions. These results are consistent with the hypothesis postulating that the peak duration of melatonin secretion is a critical parameter for transducing photoperiodic responses in pregnant or pseudopregnant mink. Secondly, they suggest that the Suprachiasmatic nuclei and the retrochiasmatic area are not essential for the action of melatonin in the photoperiodic control of prolactin and progesterone secretions during pregnancy or pseudopregnancy in the mink.
Kappa‐Opioid Receptor Involvement in the Regulation of Pulsatile Luteinizing Hormone Release During Early Pregnancy in the Rat
Authors: Gallo Robert V. 
Published: September 2006

AbstractThe object of this study was to gain further insight into endogenous opioid peptide suppression of pulsatile luteinizing hormone (LH) release in early gestation in the rat by examining whether selective blockade of mu ‐, delta ‐, or kappa‐opioid receptor(s) results in stimulation of pulsatile LH secretion at this time. Previous reports demonstrated stimulation of pulsatile LH release during early gestation by intravenous infusions of naloxone, an endogenous opioid peptide receptor antagonist whose binding is not specific to a single class of opioid peptide receptors. In the present study, naloxone infused intraventricularly similarly stimulated an increase in pulsatile LH release on Days 7 to 8 of gestation. Antagonists of specific opioid peptide receptor subtypes were thus given by this route. Administration of nor‐binaltorphimine, an antagonist of kappa‐opioid receptors, but not β‐funaltrexamine or ICI 174, 864, antagonists of mu‐ and delta‐opioid receptors, respectively, exerted a stimulatory action on both LH pulse amplitude and frequency similar to that of naloxone, indicating involvement of this opioid peptide receptor subtype in the endogenous opioid peptide suppression of pulsatile LH release in early gestation in the rat.
Effect of Naloxone on the Pulsatile Secretion of Luteinizing Hormone in Gonadectomized Male and Female Ferrets Before and After Oestradiol Replacement
Authors: Lambert G. M. , Erskine M. S. , Baum M. J. 
Published: September 2006

AbstractIntravenous infusions of the opioid receptor antagonist, naloxone, caused a significant rise in luteinizing hormone (LH) pulse frequency in male and female ferrets which had been gonadectomized 10 days earlier while in breeding condition; mean LH concentrations and LH pulse amplitudes were not affected. By contrast, naloxone failed to stimulate LH pulse frequency, or other LH parameters in gonadectomized ferrets of either sex which received daily injections of a low dose of oestradiol. Our results for the ferret, in which the female is an induced ovulator, resemble those previously obtained in another induced ovulator, the rabbit. They contrast, however, with the results of numerous studies using spontaneously ovulating species in which sex steroids, if anything, facilitate the ability of naloxone to stimulate LH secretion.
‘Peripheral’ Benzodiazepine Receptor Ligands Stimulate Prolactin Release in the Rat
Authors: Calogerot Aldo E. , Kamilaris Themis C. , Johnson Elizabeth O. , Gold Philip W. , Chrousos George P. 
Published: September 2006

AbstractHigh concentrations of ‘peripheral’ benzodiazepine binding sites have been described in the pituitary gland and in several other endocrine glands, such as the adrenal glands and the testes. The role played by these receptors on the regulation of the endocrine system is largely unknown. In this study, we report the effects of two ligands of the ‘peripheral’ benzodiazepine receptor, Ro5–4864 and PK 11195, on prolactin (PRL) release in the adult male rat. Ro5‐4864 stimulated PRL release with half maximal and maximal stimulatory doses of about 0.6 and 1.2 mg/kg, respectively. Pretreatment with the ‘peripheral’ benzodiazepine receptor antagonist PK 11195 did not have any effect on Ro5‐4864‐induced PRL release. Accordingly, PK 11195, given alone, stimulated PRL release in a dose‐dependent fashion. To examine whether the stimulatory effect of Ro5‐4864 and PK 11195 on PRL release was due to a direct effect of these compounds at the pituitary gland, we used primary cultures of anterior pituicytes. Neither Ro5‐4864 nor PK 11195 had an effect on basal PRL release nor were these agents capable of modulating thyrotropin‐releasing hormone‐stimulated or dopamine‐inhibited PRL release.These findings suggest that administration of agents that interact with the ‘peripheral’ benzodiazepine binding receptor cause PRL release without directly stimulating the pituitary gland. We speculate that Ro5–4864 and PK 11195 increase plasma PRL levels by modulating brain release of neurotransmitters and/or neuropeptides involved in the regulation of PRL release.
Involvement of Cholecystokinin in Food Intake: I. Concentrations of Cholecystokinin‐Like Immunoreactivity in the Cerebrospinal Fluid of Male Rats
Authors: Lindén A. , Uvnäs‐Moberg K. , Forsbergt G. , Bednar I. , Södersten P. 
Published: September 2006

AbstractTo investigate the role of central neural cholecystokinin in food intake the concentration of cholecystokinin‐like immunoreactivity was measured by radioimmunoassay in the cerebrospinal fluid of male rats. Characterization of the molecular forms of Cholecystokinin was made by high‐performance liquid chromatography before radioimmunoassay. Four molecular forms of cholecystokinin corresponding to standards of the tetra‐, penta‐ and sulphated octapeptide and a late eluting peak probably corresponding to cholecystokinin‐58 were found. The concentration of cholecystokinin‐like immunoreactivity in the cerebrospinal fluid decreased in response to 48 h of food deprivation and was restored after 1 h of food intake, the main increase occurring within 30 min after the onset of feeding. Cholecystokinin‐like immunoreactivity increased in the cerebrospinal fluid 10 min after an intraperitoneal injection of 5 μg cholecystokinin octapeptide, a dose which also suppressed the amount of food consumed during 1 h in rats deprived of food for 48 h. Intraperitoneal injection of the peripheral, cholecystokinin A receptor antagonists lorglumide (450 μg) or L‐364. 718 (20 μg) reversed the inhibitory effect of cholecystokinin octapeptide on food intake and prevented the increase of cholecystokinin‐like immunoreactivity in the cerebrospinal fluid. It is suggested that central neural cholecystokinin is involved in the control of food intake and that this is reflected in the alterations in cholecystokinin‐like immunoreactivity in the cerebrospinal fluid which occur in response to food deprivation and food intake. However, a variety of ways of intracerebral administration of Cholecystokinin octapeptide failed to affect food intake in food‐deprived rats. The possibility is raised that Cholecystokinin octapeptide acts in concert with another transmitter in the brain to affect food intake.
Involvement of Cholecystokinin in Food Intake: III. Oestradiol Potentiates the Inhibitory Effect of Cholecystokinin Octapeptide on Food Intake in Ovariectomized Rats
Authors: Lindén A. , Uvnäs‐Moberg K. , Forsberg G. , Bednar I. , Södersten P. 
Published: September 2006

AbstractThe role of Cholecystokinin in a model of hypophagia, oestradiol‐treated Ovariectomized rats, was investigated. Implantation of oestradiol‐filled constant‐release implants in rats made obese by ovariectomy potentiated the inhibitory effect of intraperitoneal injection of Cholecystokinin octapeptide on food intake after 24 h of food deprivation. The alterations in the concentration of Cholecystokinin in pjasma and of cholecystokinin‐like immunoreactivity in cerebrospinal fluid produced by deprivation of food for 24 h and subsequent food intake for 1 h were unaffected by the oestradiol treatment as was the amount of food consumed during 1 h. Oestradiol‐treated rats deprived of food for 6 h, however, consumed less food during a 15‐min test than controls. Treatment with oestradiol blunted the decrease in the concentration of cholecystokinin‐like immunoreactivity in the cerebrospinal fluid in response to 6 h of food deprivation. No alterations in the concentration of Cholecystokinin in plasma occurred after this period of food deprivation and subsequent feeding during 15 min in either oestradiol‐treated or control rats. Thus, treatment with oestradiol enhances responsivity to exogenous Cholecystokinin octapeptide and changes the response of endogenous levels of cholecystokinin‐like immunoreactivity in the cerebrospinal fluid to a short period of food deprivation. It is suggested that these effects are caused by an action of oestradiol on Cholecystokinin pathways in the brain. The results support the suggestion that hunger in the rat is inversely related to the decrease in the concentration of cholecystokinin‐like immunoreactivity in the cerebrospinal fluid.