bluuebunny/crossref_metadata_2025_split huggingface dataset:
Luteinizing Hormone‐Releasing Hormone and Gamma‐Aminobutyric Acid Neurons in the Medial Preoptic Area are Synaptic Targets of Dopamine Axons Originating in Anterior Periventricular Areas
Authors: Horvath Tamas L. , Naftolin Frederick , Leranth Csaba 
Published: September 2006

AbstractThe aim of this study was to characterize further the transmitter content and the location of the parent cells of tyrosine hydroxylase‐immunoreactive boutons terminating on luteinizing hormone‐releasing hormone‐ and glutamic acid decarboxylase‐immunoreactive neurons in the rat medial preoptic area. Electron microscopic immunostaining for luteinizing hormone‐releasing hormone, tyrosine hydroxylase or glutamic acid decarboxylase was performed on desipramine‐pretreated (to protect norepinephrine and epinephrine axons) rats which received a stereotaxic injection of 6‐hydroxydopamine into the medial preoptic area anteroventral periventricular nucleus 48 h prior to sacrifice. This treatment induced acute degeneration of dopamine axon terminals characterized by the development of autophagous cytolysosomes, an early morphological sign of catecholamine axon degeneration. To further define the cells of origin of these dopamine boutons, the anterograde marker Phaseolus vulgaris leucoagglutinin was iontophoretically applied to the zona incerta. Six days later, rats received a 6‐hydroxydopamine injection into the zona incerta or the lateral ventricle, and 48 h later, double immunostaining was performed for Phaseolus vulgaris leucoagglutinin and tyrosine hydroxylase, luteinizing hormone‐releasing hormone, or glutamic acid decarboxylase on preoptic area vibratome sections.Following the 6‐hydroxydopamine injection into the anteroventral periventricular nucleus, autophagous cytolysosome‐containing degenerated axons were found in synaptic contact with both luteinizing hormone‐releasing hormone and GABA neurons in the medial preoptic area, confirming that these are dopaminergic connections. Following the double injection treatment, 6‐hydroxydop‐amine‐induced degenerated, Phaseolus vulgaris leucoagglutinin‐labeled dopamine axons originating in the zona incerta were not found to contact luteinizing hormone‐releasing hormone‐containing or GABA cells. Instead, many degenerated, Phaseolus vulgaris leucoagglutinin‐immunopositive boutons were observed in the dorsomedial and paraventricular nuclei of the hypothalamus. These observations indicate that tyrosine hydroxylase‐immunoreactive fibers terminating on the medial preoptic area luteinizing hormone‐releasing hormone and GABA cells are dopaminergic and most probably originate from dopamine neurons located in anterior periventricular areas of the hypothalamus.
Lesions of the Suprachiasmatic Nucleus Indicate the Presence of a Direct Vasoactive Intestinal Polypeptide‐Containing Projection to Gonadotrophin‐Releasing Hormone Neurons in the Female Rat
Authors: van der Beek Eline M. , Wiegant Victor M. , van der Donk Hans A. , van den Hurk Rob , Buijs Ruud M. 
Published: September 2006

AbstractIn non‐seasonal breeders like the rat, the influence of the suprachiasmatic nucleus (SCN) on reproduction is most clearly expressed in the female. Complete lesions of the SCN induce persistent oestrus (anovulation) in intact female rats, whereas oestrogen implantation in ovariectomized rats results in daily luteinizing hormone surges. Vasoactive intestinal polypeptide (VIP), a peptide synthesized in cell bodies of the SCN, inhibits the increase in pulsatile luteinizing hormone release observed in ovariectomized female rats. In search of the anatomical basis for these observations, the present study employs an immunocytochemical double staining for VIP and gonadotrophin‐releasing hormone (GnRH) at the light microscopical level. It was demonstrated that approximately 45% of the GnRH positive neurons in the diagonal band of Broca, the preoptic and anterior hypothalamic area of female rats are innervated by VIP‐containing processes. To investigate whether these VIP‐containing fibres represent a direct projection of the SCN to the GnRH system, unilateral thermic SCN lesions were made.Lesions that unilaterally destroyed the majority of the VIP synthesizing cells in the SCN resulted in at least a 50% decrease of the VIP innervation of GnRH cell bodies at the lesioned side compared to the intact side. Lesions not affecting the VIP synthesizing cell population in the SCN did not change the percentage of GnRH neurons innervated by VIP‐containing fibres, while partial lesions resulted in intermediate effects.These results indicate that the majority of the light microscopical VIP‐containing input on GnRH neurons in the hypothalamus is derived from the SCN. It is suggested that the reported effects of VIP on luteinizing hormone release may, at least in part, be induced via a direct effect of VIP on GnRH cell bodies. This direct SCN‐GnRH pathway provides an anatomical basis for diurnal influences on the regulation of the female reproductive cycle.
Endogenous Catecholamines Modulate Growth Hormone Release in the Conscious Rat During Hypoglycaemia but not in the Basal State
Authors: Chapman Ian M. , Kapoor Ranjna , Willoughby John O. 
Published: September 2006

AbstractTo investigate the role of endogenous catecholamines and 5‐hydroxytryptamine in the control of growth hormone (GH) secretion, secretory profiles of GH and prolactin were measured in conscious, male rats following intravenous administration of either 1) α2 antagonist idazoxan 2 mg/kg, a dose that blocked α2 agonist induced GH rise, 2) α1 antagonist prazosin 1 mg/kg, 3) non‐specific β‐blocker propranolol 1.5 mg/kg, a dose that prevented β2 agonist (salbutamol) induced inhibition, 4) serotonin antagonist cyprohep‐tadine 0.5 mg/kg, a dose that inhibited serotonin agonist quipazine induced GH rise, or 5) control. No drug altered mean GH or prolactin levels and pulsatile GH release persisted. Unilateral injections of prazosin, propranolol and idazoxan were made into the medial basal hypothalamus and preoptic‐anterior hypothalamic area and of cyproheptadine into the medial basal hypothalamus, all with no effect on short‐term GH release. GH and prolactin secretory profiles were measured after giving rats 6 units/kg intravenous insulin. Blood glucose levels fell to less than 50% basal. Hypoglycaemia caused a non‐significant 30% fall in mean 2 h GH. Intravenous idazoxan, prazosin, propranolol and cyproheptadine (doses as in first study) did not modify the blood glucose fall, but idazoxan produced a significant reduction of mean GH compared to insulin alone (4 ± 1.1 ng/ml SEM, idazoxan/insulin versus 16 ± 5.6 ng/ml, saline/insulin). The lack of an effect of a‐ and β‐blockers on normal, pulsatile GH release is against a role for endogenous catecholamines in controlling this release. Catecholamines may be released during insulin‐induced hypoglycaemia and preferentially bind to α2 receptors to increase GH secretion, thus attenuating the suppression of GH levels that would otherwise occur.
Galanin‐Induced Growth Hormone Secretion in Conscious Rats: Evidence for a Possible Involvement of Somatostatin
Authors: Tanoh Tsutomu , Shimatsu Akira , Ishikawa Yasuhiro , Ihara Chihiro , Yanaihara Noboru , Imura Hiroo 
Published: September 2006

AbstractIntracerebroventricular administration of galanin (GAL) potently evoked growth hormone (GH) secretion in conscious male rats. Pretreatments with neostigmine and cysteamine blunted the GAL‐induced GH secretion. Pretreatment of animals with a specific anti‐somatostatin serum significantly inhibited the GAL‐induced GH secretion. On the contrary, GH‐releasing hormone‐induced GH secretion was significantly enhanced with cysteamine and anti‐somatostatin serum. These results suggest that somatostatin is involved in GAL‐induced GH secretion in rats.
In vitro Regulation of Rat Prolactin Messenger Ribonucleic Acid Poly(A) Tail Length: Modulation by Bromocriptine
Authors: Carter David A. , Li‐Jin Chew , Murphy David 
Published: September 2006

AbstractRecent analysis of endocrine gene transcripts has revealed that several hormone mRNAs exhibit regulated size changes (due to alterations in length of the 3’poly(A) tail) which may function as an additional level of control in the determination of gene expression. We have now shown, through the novel application of an organ culture technique, that prolactin mRNA exhibits a similar regulated change in poly(A) tail length when rat anterior pituitary glands are explanted. The effect is observed in glands of either male or female rats and is specific with respect to growth hormone and α‐tubulin mRNAs. Furthermore, we have also found that the size change in prolactin mRNA is attenuated in the presence of bromocriptine, indicating regulation through a dopaminergic pathway.
Molecular Identification of Two Types of lnterleukin‐1 Receptors in the Murine Pituitary Gland
Authors: Parnet Patricia , Brunke Deborah L. , Goujon Emmanuelle , Mainard Jacques Demotes , Biragyn Arya , Arkins Sean , Dantzer Robert , Kelley Keith W. 
Published: September 2006

AbstractThe present study was carried out to characterize interleukin‐1 (IL‐1) receptors on murine pituitary cells. Receptor autoradiography confirmed the existence of binding sites for IL‐1α in the murine adenphypophysis, but not in the neural or intermediate lobes. Specific binding of IL‐1 to isolated pituitary membranes revealed a Kd of 0.9 nM with a Bmax of 37 fmol/mg protein. To examine the possibility that the adenohypophysis synthesizes a receptor for IL‐1, immunocytochemistry experiments with a specific monoclonal antibody against the type I receptor revealed the existence of this protein in only the adenohypophysis. Identity of the type I IL‐1 receptor was similar to that found on T cells as determined by: 1) amplification of the predicted 619 bp fragment spanning the cytoplasmic, transmembrane and extracellular domains from RNA of pituitary and T cell origin, as well as clonal AtT‐20 pituitary cells, and 2) restriction fragment analysis and sequencing of the amplified cDNAs. The pituitary gland and AtT‐20 cells also expressed transcripts for the newly identified type II receptor for IL‐1 as assessed by amplification of a specific 325 bp fragment, restriction fragment analysis and nucleotide sequencing, and these transcripts were similar to those found on B lymphocytes. These data identify two different forms of the IL‐1 receptor in both normal and transformed pituitary calls and establish that these receptors are similar at the molecular level to those first identified on T and B lymphocytes.
Membrane Properties of Identified Guinea‐Pig Paraventricular Neurons and their Response to an Opioid μ‐Receptor Agonist: Evidence for an Increase in K+ Conductance
Authors: Kasai Masanori , Tasker Jeffrey G. , Wuarin Jean‐Pierre , Dudek F. Edward 
Published: September 2006

AbstractIntracellular recordings were obtained from neurons in the paraventricular nucleus (PVN) of guinea‐pig hypothalamic slices. Passive and active properties of the neurons were determined, and when possible, recorded neurons were injected with biocytin. The effects of a μ‐receptor opioid agonist [D‐Ala2, Nme‐Phe4, Gly5‐ol]enkephalin (DAGO) were studied in order to determine which types of cells have μ receptors and to test the hypothesis that an increase in K+ conductance causes μ‐receptor‐mediated inhibition in the PVN.The recorded cells inside the PVN were divided into two groups, primarily on the basis of the presence or absence of a low threshold Ca2+ spike (LTS). In one group of neurons, LTS potentials could not be evoked (non‐LTS cells, n = 42). In another group of neurons (n = 35), LTS potentials with one or two Na+ spikes could be initiated with depolarizing pulses superimposed on steady hyperpolarizing currents; however, these neurons did not fire robust bursts (i.e. non‐bursting LTS cells). The mean time constant of non‐LTS cells (19.9±1.6ms; mean ± SEM) was significantly shorter than that of non‐bursting LTS cells (26.7 ± 2.1 ms). There were no differences in the mean resting membrane potential, spike amplitude, spike duration, input resistance, spike threshold and pattern of synaptic inputs between the two groups. Intracellular labeling with biocytin combined with cresyl violet counter‐staining demonstrated that the two types of cells were located in the PVN. The mean diameters of non‐LTS cells along their long axis (25.4 ± 1.7 μm) and short axis (17.5 ±2.2 μm, n = 7) were larger than those of non‐bursting LTS cells (22.1 ±1.0 μm, 15.2 ± 1.1 μm, respectively, n = 12); this suggests that non‐LTS cells are magnocellular neurons and non‐bursting LTS cells are parvocellular neurons, as previously described in the rat.Bath application of DAGO at a concentration of 1 μM inhibited 7 of 25 (28%) non‐LTS cells tested, and 4 of 21 (19%) non‐bursting LTS cells. The main effect of DAGO on PVN cells was a hyperpolarization of membrane potential (4 to 15 mV) with a decrease of input resistance (20% to 38%). Quinine (100 μM to 1 mM), a K+ channel blocker, eliminated or reduced inhibitions mediated by DAGO. The apparent reversal potential of the hyperpolarization induced by the μ‐receptor agonist was about −85 mV.These data in the guinea‐pig PVN suggest that non‐LTS cells are putative magnocellular neurons, and non‐bursting LTS cells are parvocellular neurons. The μ‐receptor agonist, DAGO, directly hyperpolarizes approximately equal numbers of each of these cell types. Experiments with quinine and injected currents support the hypothesis that DAGO activation of μ receptors on neurons in the region of the PVN leads to an increase in K+ conductance.
Seasonal Variation of Neuropeptide Y Actions on Growth Hormone and Gonadotropin‐ll Secretion in the Goldfish: Effects of Sex Steroids
Authors: Peng Chun , Trudeau Vance L. , Peter Richard E. 
Published: September 2006

AbstractThe effects of neuropeptide Y (NPY) on growth hormone (GH) and gonadotropin‐II (GtH‐II) release in different reproductive stages were studied using perfused pituitary fragments of female goldfish. The GH and GtH‐II release responses to 5‐min pulses of NPY were relatively small in sexually regressed fish (July), intermediate in recrudescent fish (December), and maximal in sexually mature (= prespawning) fish (May). To test if sex steroids can modulate NPY action, the effects of in vivo implantation of 17β‐estradiol (E2) and testosterone (T) (both at 100 μg/g dosage) on NPY‐induced GH and GtH‐II secretion were examined. In sexually regressed goldfish, implantation of T significantly enhanced NPY‐induced GH and GtH‐ll release from perfused pituitary fragments; implantation of E2 potentiated the NPY‐induced GtH‐II, but not GH release. However, steroid implantation did not affect responses to NPY when this experiment was repeated using pituitaries from sexually mature fish. To test the hypothesis that steroids may act directly at the level of the pituitary to potentiate NPY action, pituitary fragments taken from sexually regressed goldfish were incubated with 100 nM T for 24 h, and the GH and GtH‐ll responses to 5‐min challenges of NPY assessed in the presence of T. Both GH and GtH‐ll responses to NPY were not affected by treatment with T in vitro, suggesting that T does not act directly at the level of the pituitary. Since we have found that gonadotropin‐releasing hormone (GnRH) in part mediates the effects of NPY on GH and GtH‐ll release, the possibility that steroids may potentiate the actions of NPY on GnRH release were also examined. In sexually regressed fish, NPY did not alter GnRH release either from pituitary fragments or preoptic anterior hypothalamic slices. When fish were pretreated with E2 and T by in vivo implantation, NPY significantly stimulated the release of GnRH. Taken together, these results demonstrate that: 1) there is a seasonal variation of NPY action on GH and GtH‐ll release in the female goldfish; 2) sex steroids, especially T, potentiate the effects of NPY on GH and GtH‐ll release in sexually regressed fish, when the endogenous steroid levels are low; and 3) the seasonality of NPY actions and the potentiation by steroids may be mediated, at least in part, by enhanced stimulation of GnRH release.
Estrogen Receptor Immunostaining in the Preoptic Area and Medial Basal Hypothalamus of Estradiol Benzoate‐ and Prazosin‐Treated Female Guinea‐Pigs
Authors: Malik Karl F. , Feder Harvey H. , Morrell Joan I. 
Published: September 2006

AbstractEvidence has accumulated showing that the α1‐adrenergic antagonist prazosin decreases nuclear estrogen binding in the hypothalamus of the guinea‐pig. In this study we asked if prazosin treatment alters estrogen receptor (ER) protein content as reflected by changes in ER‐immunoreactivity. The monoclonal rat antibody H222 directed against ER was used to detect ER‐immunoreactive (ER‐ir) cells in eight specific preoptic and hypothalamic brain regions of ovariectomized Hartley strain guinea‐pigs treated with estradiol benzoate and 1.0mg/kg prazosin or vehicle. Immunocytochemical parameters which provided optimum conditions for detection of even modest changes in ER‐immunoreactivity were first established. Then, using these optimum conditions, we compared 1) the mean number of ER‐ir profiles, 2) the mean density of ER‐ir staining, and 3) the distribution of ER‐ir staining density readings, between conditions within each of the eight brain regions. No differences in any of these measures were found between prazosin‐ and vehicle‐treated females. We also compared the percentage of ER‐ir nuclear profiles across the eight cell groups investigated in estradiol benzoate‐ and vehicle‐treated females. The medial preoptic area had by far the highest percentage (48%) of ER‐ir profiles (P<0.05) compared to all seven other brain regions (23% to 32% ER‐ir cells). Our data, showing that ER‐immunoreactivity is not reduced (6 h) after prazosin treatment, suggests that mechanisms other than alterations in ER protein should be considered when interpreting the effects of prazosin on the retention of estradiol by nuclear or cytosolic extracts of hypothalamic lysates.
Sexual Dimorphism in the Distribution of a‐Neoendorphin‐Like Immunoreactivity in the Anterior Pituitary of the Rat
Authors: Bello Aixa R. , Kah Olivier , Croix Dominique , Ciofi Philippe , Tramu Gérard 
Published: September 2006

AbstractThe localization of the opioid peptide α‐neoendorphin (α‐Neo‐E) was studied in the anterior pituitary of normal and castrated male and normal female rats, Immunoreactive (ir) cells were noted in both sexes. These α‐Neo‐E‐ir cells were further characterized using double immunostaining with an elution‐restaining procedure. It was seen that in males, α‐Neo‐E‐ir cells corresponded mainly to luteinizing hormone/follicle‐stimulating hormone cells and a few thyroid‐stimulating hormone (TSH) cells, whereas in females, virtually all α‐Neo‐E‐ir cells corresponded to TSH cells.Castration of male rats caused, within 3 to 5 days, a dramatic decrease in the number of α‐Neo‐E‐ir gonadotrophs, whereas the number of a‐Neo‐E‐ir TSH cells tended to increase. Two weeks after castration, however, most α‐Neo‐E‐ir cells were also follicle‐stimulating hormone‐ir.This study demonstrates that in the anterior lobe of the rat, α‐Neo‐E‐ir is located within gonadotrophs and/or thyrotrophs, depending on the sex. In addition, results obtained following castration suggest that the expression of this peptide in the anterior pituitary depends upon the steroid environment, possibly indicating that α‐Neo‐E is implicated in the regulation of the pituitary‐gonadal axis.
Concomitant Changes of Messenger Ribonucleic Acid Levels of Secretogranin II, VGF, Vasopressin and Oxytocin in thé Paraventricular Nucleus of Rats After Adrenalectomy and During Lactation
Authors: Mahata S. K. , Mahata M. , Hörtnagl H. , Fischer‐Colbrie R. , Steiner H.‐J. , Dietze O. , Winkler H. 
Published: September 2006

AbstractIn situ hybridization was used to study the mRNA levels for secretogranin II and VGF in comparison with those of oxytocin and vasopressin in the hypothalamus of rats. VGF is a widespread constituent of large dense core vesicles which is selectively induced in PC12 cells by nerve growth factor. After adrenalectomy the mRNA levels of secretogranin II, VGF and vasopressin were increased 4‐ to 5‐fold in the parvocellular neurons of the paraventricular nuclei. In lactating rats the message for oxytocin and secretogranin II were significantly elevated in the magnocellular neurons of the paraventricular and supraoptic nuclei, whereas for VGF only a smaller non‐significant increase was observed. As shown by immunoelectron microscopy secretoneurin (a peptide derived from secretogranin II) and oxytocin are co‐stored in the large dense core vesicles of the hypothalamo‐neurohypophysial neurons.These results demonstrate that stimulation of both parvo‐ and magnocellular neurons of the hypothalamus induces a concomitant increase of the messages for secretogranin II and VGF together with those of vasopressin and oxytocin.
Denervation of the Rat Posterior Pituitary Gland: Validation of a Stereotaxic Method
Authors: Makara G. B. 
Published: September 2006

AbstractA stereotaxic surgical method was developed for interrupting the nerve fibres running through the rat pituitary stalk to the posterior pituitary gland without obliterating the hypothalamo‐pituitary portal circulation. The pituitary stalk was compressed by the blunt tip of an L‐shaped rotating knife. Successful operations produced mild diabetes insipidus, disappearance of arginine vasopressin from the neural lobe, accumulation of arginine vasopressin and neurosecretory material in the pituitary stalk and no infarction in the anterior lobe of the pituitary gland. In female rats, the oestrous cycle was only temporarily disturbed. Plasma prolactin and corticosterone levels were high during the first 24 h after the stalk compression but returned to normal baseline levels from the second day after the operation. One week after the operation plasma adrenocorticotropin and prolactin levels were in the control range while plasma a‐melanocyte‐stimulating hormone was elevated. Denervation of the posterior pituitary gland may help in studying the neural control of intermediate lobe function and the role of the neural lobe in various endocrine conditions, and may serve as a model for lesions of the pituitary stalk and formation of ectopic neurohypophysis in the human.