bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mu‐Selective Opioid Peptides Stimulate Prolactin Release in Lactating Rats
Authors: Baumann Michael H. , Rabii Jamshid 
Published: September 2006

AbstractThe fact that opiates elicit prolactin secretion is well known. However, we have recently discovered that morphine does not stimulate prolactin release in lactating rats. The physiological basis for this alteration in opiate sensitivity during lactation is not known. Since morphine‐induced prolactin secretion in male rats is mediated via the mu opioid receptor subtype, one possible explanation is that mu receptors are down‐regulated during lactation. To address this possibility, the effects of mu opioid peptides on prolactin secretion were examined in lactating rats. The presumed mu‐selective peptides DAGO ([D‐Ala2, Me‐Phe4, Gly‐ol5]‐enkephalin) and PLO‐17 ([NMe‐Phe3, D‐Pro4]‐morphiceptin) were administered to primiparous lactating rats and the resulting hormone responses measured. Both DAGO and PLO‐17 caused a rapid and significant rise in plasma prolactin during lactation. The prolactin‐releasing effects of both peptides were naloxone reversible, suggesting involvement of opioid receptors. Moreover, the DAGO‐induced secretion of prolactin could be completely abolished by pretreatment with the irreversible mu antagonist β‐funaltrexamine. In lactating rats, DAGO and PLO‐17 were poor growth hormone‐releasing agents, providing further evidence for the mu specificity of these peptides. These results imply that during lactation, as in other reproductive states, mu opioid receptor sites are positively coupled to the prolactin secretory mechanism. Thus, the previously observed inability of morphine to elicit prolactin release in lactating rats cannot be explained on the basis of down‐regulation of mu opioid receptors.
Identification and Localization of Insulin‐Like Growth Factor Receptors in Human Infant Pituitary Gland—Similar Distribution to Somatotrophs
Authors: Walker David A. , Hogg Annette , Haynes Kerry , Cox Alison , Jonas Helen , Mendelsohn Frederick A. O. , Werther George A. 
Published: September 2006

AbstractInsulin‐like growth factors(IGF) are involved in feedback regulation of growth hormone(GH) secretion from the pituitary. Though receptors for IGF‐I and IGF‐II have been identified on particulate preparations of rat pituitary, their localization and relationship to GH‐secreting acidophils has not been determined. We used quantitative in vitro autoradiography and immunocytochemistry to simultaneously determine the distribution of IGF receptors and GH‐secreting cells in human infant pituitary gland. Frozen or fixed post‐mortem human infant pituitary glands were sectioned for binding studies, or immunocytochemistry. Binding for IGF‐I and IGF‐II showed characteristic specificity for respectively Type I and Type II receptors. Binding sites were visualized throughout the pituitary gland, with similar density and distribution for IGF‐I and IGF‐II receptor sites. Receptor density was two‐fold higher in anterior than posterior pituitary, with highest density in the lateral horns of the anterior pituitary. The distribution of GH‐containing cells (acidophils) was similar to IGF receptor distribution. Increased density of IGF receptors in regions of GH‐secreting cells may point to the mechanism whereby IGF uniquely inhibits synthesis of human GH in contrast to its promotion of synthetic processes in other cells.
The Origin and Regulation of Posterior Pituitary Vasopressin Ribonucleic Acid in Osmotically Stimulated Rats
Authors: Levy Andy , Lightman Stafford L. , Carter David A. , Murphy David 
Published: September 2006

AbstractVasopressin ribonucleic acid (VP RNA) accumulates in the posterior lobe of the rat pituitary in response to an osmotic stimulus. The accumulation of posterior pituitary VP RNA can be prevented by stalk transection or the intracerebroventricular injection of colchicine. The hypothalamic and pituitary VP RNAs however, have different structures and are independently regulated. Depletion of serotonin with parachlorophenylalanine blocks the osmotically induced accumulation of both VP and oxytocin RNA in the hypothalamus but does not affect the accumulation of VP RNA in the posterior pituitary gland. In Brattleboro rats, posterior lobe oxytocin RNA but not VP RNA, increases after osmotic stimulation. Although axonal transport of RNA may occur, our results are also consistent with VP RNA synthesis in pituicytes controlled by hypothalamic neuroendocrine factors released by neurohypophyseal terminals in response to osmotic stimuli.
Activation of Opioid Receptors in the Mediobasal Hypothalamus Stimulates Prolactin Secretion in the Conscious Rat
Authors: Kapoor Ranjna , Willoughby John O. 
Published: September 2006

AbstractIn an attempt to localize the opioid receptor(s) (mu, delta and kappa) involved in opioid‐stimulated prolactin release in the conscious male rat, opioid agonists were microinjected into the mediobasal hypothalamus and prolactin levels measured before and after injection.The specific mu agonist, DAGO ((D‐Ala2, NMe‐Phe4, Gly‐ol5)‐enkephalin) was the most effective in eliciting prolactin release, the smallest effective dose being 0.01 nmoles. The specific delta agonist, DPDPE ((D‐Pen2, D‐Pen5)‐enkephalin) had no significant effect even at the highest dose of 10 nmoles. The specific kappa agonist, U50,488H ((trans‐3,4‐dichloro‐N‐methyl‐N‐(2‐(1‐pyrrolidinyl)‐cyclohexyl)‐benzene acetamide) was effective at the doses 1.0 and 10 nmoles.We conclude that mu and kappa opioid receptors in the mediobasal hypothalamus are involved in opioid‐stimulated prolactin release and that delta receptors are not.
Neuronal Uptake of Monoclonal Anti‐Vasopressin Antibodies in vivo and Relationship with the Physiological Status of Vasopressin Neurosecretory Cells
Authors: Burlet A. , Arahmani A. , Tankosic P. , Burlet C. 
Published: September 2006

AbstractMouse monoclonal anti‐vasopressin antibody was injected just above one hypothalamic paraventricular nucleus of the rat brain. Immunocytochemistry and morphometric analysis showed that the antibody was taken up by neurons with the size and stereotaxic distribution of vasopressin‐producing neurons. Labelled neurons were counted with an electronic image analyser. When the rats were deprived of drinking water for 48 h before injection, specific uptake was significantly increased in the caudal part of the nucleus. Conversely, rehydration following dehydration or chronic treatment with 1‐deamino‐8‐D‐arginine vasopressin significantly decreased neuronal uptake, mainly in the rostral subdivision of the nucleus. By contrast, bilateral adrenalectomy performed 2 weeks before injection did not modify the number of labelled magnocellular neurons, though the accumulation of injected antibody in the external layer of the median eminence indirectly demonstrated the stimulation of antibody uptake by parvocellular vasopressin neurons.The number of labelled neurons was therefore directly related to the physiological state of the vasopressin‐producing neurons. Further investigations will have to be performed to prove that the immunological targeting of peptidergic neurons offers a new tool to act in vivo on central neurons.
Anatomical Localization of Corticotropin‐Releasing Factor and Arginine Vasopressin in the Human Hypothalamus; the Effect of Corticosteroids on their Concentrations in Human and Rat Hypothalami
Authors: Pralong François P. , Linton Elizabeth A. , Favrod‐Coune Charles A. , Lowry Phillip J. , Muller Alex F. , Gaillard Rolf C. 
Published: September 2006

AbstractIn this study, we have determined the distribution of corticotropin‐releasing factor and vasopressin in the human hypothalamus, and investigated the effect of glucocorticoid administration on the concentrations of both peptides. Corticotropin‐releasing factor and vasopressin were measured by a two‐site immunoradiometric assay and/or radioimmunoassay. The presence of both peptides was studied in extracts of eleven areas of the human hypothalamus as well as in the pituitary stalk from autopsied patients who had been free of chronic steroid administration (n = 14) or had received Corticosteroids (n = 5). Unlike vasopressin, corticotropin‐releasing factor was detected in all extracts: the highest concentration was found in the pituitary stalk, whilst the lowest detectable amounts occurred in the supraoptic and lateral areas and in the mammillary bodies. This pattern of distribution is similar to that reported for the rat hypothalamus. The excellent correlation (R = 0.994) between corticotropin‐releasing factor data obtained by immunoradiometric assay and by radioimmunoassay renders the presence of a corticotropin‐releasing factor precursor molecule in the extracts highly unlikely. In the human brain extracts, glucocorticoid treatment affected neither the content, nor the distribution of corticotropin‐releasing factor and vasopressin. In the rats, dexamethasone administration produced a 50% decrease in the vasopressin content (P < 0.05) of the basomedial and dorsal parts of the hypothalamus and had no effect on the corticotropin‐releasing factor content of these areas. These results show that the distribution of corticotropin‐releasing factor is similar in both human and rat hypothalami. The rat data suggest that negative feedback effects of glucocorticoids involve changes in hypothalamic vasopressin content.
Central Oxytocin Stimulates Luteinizing Hormone Release in the Marmoset, a Primate which Fails to Show Lactationally‐lnduced Infertility
Authors: O'Byrne K.T. , Lunn S. F. , Coen C. W. 
Published: September 2006

In several species, including humans, suckling is known to suppress pulsatile gonadotrophin secretion and substantially reduce fertility (1). During suckling high titres of oxytocin are present in both plasma (2, 3) and cerebrospinal fluid (CSF) (4) and there is some evidence that oxytocin is inhibitory to gonadotrophin secretion by an action on t h e central nervous system, (5, 6). The common marmoset, however, has a different physiological response and fails to show lactational infertility; ovarian cyclicity is resumed immediately post‐partum (7). We have therefore examined the effect of centrally administered oxytocin on luteinizing hormone (LH) secretion in this species.We report that LH release was stimulated with a rapid:esponse and in a dose‐dependent manner by oxytocin injected into t h e third cerebral ventricle. In contrast, oxytocin administered intravenously was without effect on LH secretion. These results clearly indicate, for the first time, a stimulatory role for oxytocin in LH secretion in the marmoset, a species which fails to demonstrate lactational infertility.
Arachidonate Metabolism in the Anterior Pituitary: Effect of Arachidonate Inhibitors on Basal and Stimulated Secretion of Prolactin, Growth Hormone and Luteinizing Hormone. I. Hormone Release from Incubated or Perifused Pituitary Fragments
Authors: Wandscheer Dolores E. , Bihoreau Claire , Bertrand Philippe , Clauser Hubert , Kordon Claude 
Published: September 2006

AbstractThe potential involvement of arachidonic acid metabolites in the regulation of adenohypophyseal secretion was analysed on pituitary glands from male rats incubated in the presence of various inhibitors with different mechanisms of action: two inhibitors of phospholipase A2 (parabromophenacylbromide, PB and compound CB 874), an inhibitor of cyclooxygenase‐ and lipoxygenase‐catalysed pathways (5, 8, 11, 14‐eicosatetraynoic acid, ETYA) and an inhibitor of cyclooxygenase (ε‐lysyl acetylsalicylate, ASP). Under conditions which minimize side effects of the drugs, all inhibitors reduced prostaglandin synthesis and release, without affecting the metabolic integrity of the tissues (assessed by their intracellular adenosine triphosphate levels).All agents tested (PB, ETYA, ASP) suppressed prolactin secretion induced either by thyrotropin‐releasing hormone or vasoactive intestinal peptide. Basal prolactin secretion was sensitive to phospholipase A2 inhibitors. Similar inhibitions were obtained with ETYA and CB 874 on growth hormone secretion under basal conditions as well as after stimulation by growth hormone‐releasing factor, thyrotropin‐releasing hormone, or vasoactive intestinal peptide.In contrast, luteinizing hormone secretion, stimulated or not by gonadotropin‐releasing hormone, was not sensitive to any of the agents used.It is concluded that, in intact male hemipituitaries, arachidonic acid metabolism is involved in the stimulation of prolactin and growth hormone secretion by neuropeptides. In contrast, luteinizing hormone release does not seem to depend on that mechanism. It has been verified that the inhibitors of arachidonic acid metabolism do not directly interfere with adenylate cyclase, or with the activation of protein kinase C, two enzymes which are involved in the regulation of secretory mechanisms.
Progestin Receptor Induction and Sexual Behavior by Estradiol Treatment in Male and Female Rats
Authors: Coirini Héector , McEwen Bruce S. 
Published: September 2006

AbstractSex differences in the induction of cytosolic progestin receptors (CPR) by estrogen priming were correlated with the sex differences in behavioral responses. We evaluated the temporal relationship between CPR in several brain regions and pituitary and the time‐course of 17β‐estradiol (E2) activation of female sexual behavior in gonadectomized male and female rats implanted with subcutaneous E2 Silastic capsules for 6 h, 24 h and 48 h. Both CPR levels and mating behavior increase monotonically with the time of E2 exposure. Induction of CPR was observed in the periventricular region of the preoptic area (PVPOA), arcuate nucleus (ARC), ventromedial nuclei (VMN) and pituitary in both sexes. A small induction of CPR was found in parietal cortex. The VMN in female rats showed a significant E2‐induced CPR increase at all times of exposure, while in male rats this induction was only significant after 24 h. Significant sex differences in absolute CPR levels and E2‐induced receptors were found in the following structures: VMN, 18 h after 6 h of E2 treatment and after 24 h and 48 h of continuous E2 exposure; PVPOA, only after 48 h of continuous E2 exposure; ARC at 24 h and 48 h; and pituitary after all E2 treatment. Mating behavior was tested under two conditions: E2 alone (2 h after removal of E2 capsules) and E2+progesterone (2 h after a progesterone injection given 10 min after concluding the first test). Receptivity was first observed after 24 h E2 exposure in female rats, whereas in male rats a small response appeared only after 48 h of E2 exposure. After progesterone priming, the time of E2 exposure necessary for expression of female sexual behavior was reduced to 6 h in females and 24 h in males. The appearance of mating behavior appears to follow that of inducible CPR in the VMN in both sexes. In addition, the CPR levels associated with the first receptivity either by male rats (16.6 fmol/mg protein) or female rats (15.3 fmol/mg protein) are very similar suggesting the presence of a threshold level controlling the expression of feminine sexual behavior. It is likely that inhibitory neural input plays a role in determining the threshold level of E2‐induced CPR, which is sufficient to trigger lordosis behavior.
Effects of Cysteamine Pretreatment and Hypothalamic Periventricular Nucleus Lesion on the Cold‐Stimulated Thyrotropin Responses to Intracerebroventricular 5‐Hydroxytryptamine in Male Rats
Authors: Toivonent M. , Tuomainen P. , Rauhala P. , Männistö P. T. 
Published: September 2006

AbstractThe hypothalamic somatostatinergic system was devitalized in male rats by intracerebroventricular (icv) cysteamine (CSH) pretreatment (250 μg/rat/day into the third ventricle) on 4 consecutive days or by a limited lesion of the hypothalamic periventricular nucleus (PeVNx). The acute effect of icv serotonin (5‐HT) on the cold‐stimulated thyrotropin (TSH) and prolactin responses were studied in these animals. The experiments were performed 24 h after the last saline or CSH infusions and 7 days after the sham‐ or PeVN‐lesions. CSH and PeVNx decreased the hypothalamic somatostatin content by 44% to 57% and 19% to 28%, respectively. PeVNx did not affect hypothalamic thyrotropin‐releasing hormone content. 5‐HT infusion (9 μg/rat icv) into the anterior third ventricle elevated, although not significantly, TSH levels in both saline‐ or CSH‐pretreated rats. 5‐HT infusion into the anterior third ventricle did not affect TSH in sham‐operated rats. However, 5‐HT augmented the cold‐stimulated TSH levels after PeVNx compared to sham‐lesion. Inversely, 5‐HT infusion (9 μg/rat) into the posterior third ventricle inhibited TSH secretion irrespective of the pretreatment or lesion. The inhibitory action of 5‐HT on TSH was significantly suppressed by CSH. 5‐HT infusions elevated serum prolactin levels irrespective of the infusion site, pretreatment or lesion. 5‐HT infusion into both the anterior and the posterior third ventricle decreased rectal temperature in saline‐pretreated, sham‐ and PeVN‐lesioned rats. The hypothermie effect of 5‐HT was weakened by CSH. The hypothalamic levels of noradrenaline, dopamine and their metabolites were not significantly affected by CSH and PeVNx. 5‐HT infusion into the anterior third ventricle decreased hypothalamic dopamine content in both saline‐ and CSH‐pretreated rats. However, such an effect was not seen in sham‐ or PeVN‐lesioned animals. Although CSH is an inhibitor of dopamine‐β‐hydroxylase, this activity was not reflected in serum TSH or prolactin levels. The results support our hypothesis of the site‐dependent action of icv 5‐HT or TSH secretion. The elevation of TSH levels may arise from the inhibition of somatostatin release from rostral anterior hypothalamus. The inhibition of TSH secretion may result from the inhibition of thyrotropin‐releasing hormone release from more caudal periventricular structures of the hypothalamus.
Effects of Stimulation of the Superior Cervical Ganglia and Local Application of Noradrenaline on Electrical Activity of the Syrian Hamster Pineal Gland
Authors: Patel S. , Demaine C. 
Published: September 2006

AbstractThe effects of electrical stimulation of either or both superior cervical ganglia and the effects of local application of L‐noradrenaline on the spontaneous electrical activity of hamster pineal cells were evaluated. Extracellular recordings from pineals of anaesthetized hamsters revealed that the spontaneous electrical activity was mainly regular with interspike intervals attributed between 12 to 20 ms during the daytime and mainly irregular with interspike intervals of 1 to 250 ms during the night. Following stimulation of the superior cervical ganglia, either unilaterally or bilaterally, or local application of noradrenaline, the responses of these pineal cells fell into three major categories: A) non‐responsive, B) excited, and C) inhibited. There was no relationship between the magnitude or form of response and the source of stimulus i.e. the right superior cervical ganglia or the left superior cervical ganglia. Almost all inhibited responses from electrical stimulation of the superior cervical ganglia could be correlated with inhibited responses from the local application of noradrenaline whereas excited responses could not. In general, these results suggest that the spontaneous electrical activity of some pineal cells is influenced by inputs from the superior cervical ganglia and that the inhibitory input is likely to be mediated through the release of noradrenaline. The excitatory input from the superior cervical ganglia is probably mediated by another neurotransmitter. The heterogeneity of responses suggests that different receptors or different cell types may be involved.
Temperature and Protein Kinase C Modulation of Gonadotropin‐Releasing Hormone Receptors in Pituitary Cells from Intact or Castrated Male Rats
Authors: Leblanc Pierre , Haour France , I'Heritier Andrée , Mounier Françoise , Kordon Claude 
Published: September 2006

AbstractBinding constants of [125 I]Des‐Gly10‐(D‐Ala6)‐gonadotropin‐releasing hormone‐ethylamide (GnRHa) to dispersed pituitary cells were evaluated in a 4‐day culture. Cells were sampled either from intact or from castrated male rats and binding was measured at various temperatures before or after treatment with phorbol‐12‐myristate‐13‐acetate (PMA) or 1‐5‐(isoquinolinyl‐sulfoxyl) 2‐methylpiperazine (H7), which activate or inhibit, respectively, protein kinase C (PKC). In cells from intact rats incubated with increasing concentrations of ligand at 21 °C for 25 min, the Scatchard plot was not linear and calculation of the Hill coefficient (NH) was indicative of positive cooperativity (NH= 1.26 ± 0.02). Such non‐linearity was not observed when cells were incubated at 0.5 °C for 3 h. In that condition the maximal number of binding sites measured at equilibrium (Bmax) increased (15.1 ± 0.05 versus 9.3 ± 0.5 fmoles × mg−1 proteins at 21 °C). Two control experiments permitted us to rule out the possibility that lower Bmax at 21 °C might reflect internalization: 1) Cells were first incubated with the ligand at 21 °C for 25 min and subsequently for 3 additional hours at 0.5 °C. Preincubation did not affect the Bmax obtained at 0.5 °C; 2) when the radioligand bound to the cell surface was washed out with an acidic buffer, only 13% of the specific radioactivity was retained irrespective of the ligand concentration applied, a much lower value than the 40% binding difference observed between 0.5°C and 21°C. When the cells were incubated with PMA, the Scatchard plot was linearized and the Bmax recorded at 21 °C increased by 50% over control cells (13 ± 0.7 fmoles × mg−1 proteins). Conversely, inhibition of PKC by H7, a preferential PKC inhibitor, was ineffective. In contrast, cells sampled from castrates exhibited linear and comparable Scatchard plots at either 0.5 ° or 21 °C, with Bmax values of 14.4 ± 0.3 and 15 ± 0.34 fmoles × mg−1 proteins, respectively. PKC activation did not affect binding in that model, but H7 decreased the number of sites (Bmax= 10.7 ± 0.9) and induced appearance of positive cooperativity (NH= 1.36 ± 0.07). Taken together, these experiments reveal a pool of GnRH receptors in the pituitary of intact rats that recognizes the ligand in a phosphorylation‐dependent manner. These binding sites also became evident when biological properties of the membrane were modified by temperature or cell homogenization. After castration, PKC activation was no longer a prerequisite for recruitment of the total population of receptors whereas protein kinase inhibition resulted in a reduction of maximal binding. Finally, our observations demonstrate that GnRH binding can exhibit positive cooperativity, either on normal cells or on cells from castrates after protein kinase inhibition, suggesting that such a cooperativity is not related to a GnRH‐dependent phosphorylation.