bluuebunny/crossref_metadata_2025_split huggingface dataset:
Interaction of Opiate Peptides with Dopamine Effects on Prolactin Secretion and Membrane Electrical Properties in Anterior Pituitary Cells from Lactating Rats
Authors: Enjalbert A. , Israel J. M. , Zhang J. , Kordon C. , Vincent J. D. 
Published: September 2006

AbstractMet‐enkephalin and β‐endorphin induced a partial reversion of the dopamine inhibition of prolactin release from pituitary cells of lactating rats in primary culture. This effect of opiate peptides was dose‐dependent with an EC50 of 40 ± 8 nM and 45 ± 7 nM and maximal blockade of dopamine inhibition of 60% and 68% for Met‐enkephalin and β‐endorphin, respectively. Naloxone antagonized the effect of Met‐enkephalin with an EC50 of 22 ± 12 nM. Furthermore, this Met‐enkephalin effect on dopamine inhibition of prolactin secretion appeared non‐competitive since it reduced maximal inhibition without affecting the apparent affinity of dopamine. Finally, it should be noted that the two opiate peptides had no effect on spontaneous prolactin release.In electrophysiological experiments, local ejection of dopamine on tested cells induced an hyperpolarization concomitant with an increase of the membrane conductance. Ejection of Met‐enkephalin or β‐endorphin alone did not modify the electrical properties of the cells (resting potential, membrane conductance and excitability). In contrast, both peptides blocked in a reversible manner the dopamine‐induced electrical responses. These effects were antagonized by naloxone. However, this interaction of opiatepeptides with dopamine electrical response was not observed on all cells tested. We conclude that the blocking effect of opiates on dopamine‐induced hyperpolarization may account, at least in part, for the ability of these peptides to interact with dopamine inhibition of prolactin release.
Estrogens Modulate the Responsiveness of in vivo Recorded Striatal Neurons to lontophoretic Application of Dopamine in Rats: Role of D1 and D22 Receptor Activation
Authors: Demotes‐Mainard J. , Arnauld E. , Vincent J. D. 
Published: September 2006

AbstractEstrogens are known to affect the functioning of the extrapyramidal motor system. Their actions concern both pre‐ and postsynaptic components of the dopaminergic nigrostriatal neurotransmission. Postsynaptically, estradiol alters the electrophysiological responses of striatal neurons to dopamine application. The aim of this study was to determine the respective roles of D1 and D2 receptor subtypes in this modification of dopamine action. Eighty‐three spontaneously firing caudate neurons of ovariectomized female rats were extracellularly recorded during iontophoretic ejection of dopamine or dopaminergic agonists or antagonists. Between 5 and 10 h after a single 17β‐estradiol injection (60 μg/kg), the predominant effect of dopamine was an activation of firing (63%), and the distribution of responses significantly differed from controls and from neurons recorded less than 5 h after estradiol injection (P<0.001) on which dopamine mainly elicited inhibitory effects (71% and 63%, respectively). The excitatory effects of dopamine on this subset of spontaneously firing striatal neurons were blocked by the D1 antagonist SCH 23390 (56%), whereas the inhibitory actions were antagonized by sulpiride (62%), whose isolated application often had an excitatory effect (54%).The distributions of the responses to specific D1 or D2 agonists were not altered by estrogen treatment: the predominant effect of the D2 agonist RU 24213 was in all groups a reduction of firing rate (54%), and the D1 agonist SKF 38393 mainly induced either a decrease in mean firing rate (21%) or a biphasic effect consisting on an excitation‐inhibition sequence (53%).These results suggest that estradiol does not qualitatively alter the coupling of D1 or D2 receptors to their electrophysiological effectors, but rather quantitatively changes the ratio between the D1 and D2 receptor‐mediated components of dopamine actions, reinforcing the D1 and/or attenuating the D2 receptor‐mediated component.
Specific Physiological Regulation of Luteinizing Hormone Secretory Events Throughout the Human Menstrual Cycle: New Insights into the Pulsatile Mode of Gonadotropin Release
Authors: Sollenberger Michael J. , Carlsen Elisabeth C. , Johnson Michael L. , Veldhuis Johannes D. , Evans William S. 
Published: September 2006

AbstractTo investigate the physiological regulation of luteinizing hormone (LH) secretory events and the endogenous clearance of this hormone, we applied multiple‐parameter deconvolution analysis to serum LH concentration‐time series obtained from normal women during three phases of the menstrual cycle. The number of significant LH secretory bursts (/24 h) was maximal in the late follicular (LF) phase (27 ± 1.6; mean ± SEM), minimal in the mid‐luteal (ML) phase (10 ±1.0) and intermediate in the early follicular (EF) phase (18 ± 1.4). Similarly, the half‐duration of the secretory impulse (min) was different at each phase of the cycle with values of 6.5±1.0, 3.5±0.9 and 11 ± 1.1 during the EF, LF and ML phases, respectively. In contrast, there were no cycle‐dependent differences in the LH half‐life or in the total daily secretion of LH.When maximal secretory impulse amplitudes were examined, a putative bimodal distribution was found in the ML but not the EF or LF phases. The amplitudes for the large ML impulses, the LF and EF impulses and the small ML impulses were 0.95 ± 0.05, 070 ± 0.03, 0.43 ± 0.02 and 0.26 ± 0.02, respectively. The mass (mlU/ml) of hormone secreted within bursts was minimal in the LF phase (2.1 ± 0.1), maximal in the large ML impulses (10.2 ± 0.5) and intermediate in the EF (2.8 ± 0.1) and small ML (3.1 ±0.3) secretory impulses.There was no evidence of tonic (i.e. inter‐secretory burst) LH secretion during any phase of the menstrual cycle. The early morning hours of the EF phase were characterized by fewer secretory bursts of greater amplitude. During the ML phase, autocorrelation analysis of inter‐secretory burst intervals revealed a negative association indicating that high frequency events both precede and follow secretory pauses. In addition, secretory burst amplitude and both the preceding and following inter‐secretory burst interval was correlated to secretory burst amplitude.These new data on the nature of regulated LH secretion indicate that specific facets of spontaneous LH secretory events are controlled throughout the menstrual cycle. Such observations offer a basis for defining altered secretory dynamics in a variety of pathophysiologic situations.
The Effects of Rat Corticotrophin‐Releasing Factor‐41 Peptide Fragments on Bioassay and Immunoassay Determination of Corticotrophin‐Releasing Factor‐41 Levels
Authors: Milton N. G. N. , Nicholson S. A. , Self C. H. , Hillhouse E. W. 
Published: September 2006

AbstractPeptide fragments of rat corticotrophin‐releasing factor‐41 (CRF‐41) containing amino‐acid residues 21–33 antagonized the 5 nmol/l CRF‐41‐stimulated adrenocorticotrophin secretion from the adult rat pituitary gland in vitro. The CRF 6‐33 sequence had antagonistic effects at equimolar (5 nmol/l) concentrations which were not observed at high (50 nmol/l) concentrations whilst the CRF 21–41 sequence had effects only at high (50 nmol/l) concentrations. Similar effects were observed with CRF 6‐33 on basal release of adrenocorticotrophin. Peptide fragments elevated radioimmunoassay measurement of CRF‐41 whilst inhibiting measurement of CRF‐41 in a two‐site enzyme amplified immunometric assay. The inhibitory effects of peptide fragments in the enzyme amplified immunometric assay could be removed by dilution to within the lower end of the standard curve or by increasing the concentration of antibody bound to the solid phase. These inhibitory effects mimic those of peptide fragments on basal adrenocorticotrophin release seen in a rat pituitary gland in vitro bioassay indicating that such two‐site immunoassay determinations bear closer relation to bioactivity than those obtained using radioimmunoassay.
Differential Mechanisms of Dopamine and Somatostatin Inhibition of Prolactin Secretion from Anterior Pituitary Cells
Authors: Musset F. , Bertrand P. , Priam M. , Kordon C. , Enjalbert A. 
Published: September 2006

AbstractThe relative potencies of dopamine and somatostatin to inhibit prolactin secretion by pituitary cells in primary culture were compared. Hormone secretion was evaluated under basal conditions as well as after challenging it with thyrotropin‐releasing hormone, vasoactive intestinal peptide or with drugs affecting either the activity of adenylate cyclase (forskolin), and protein kinase C (phorbol 12 myristate 13 acetate), or eliciting Ca2+ fluxes in the cell by various ways (A23187, a Ca2+ ionophore, the dihydropyridine agonist BAY‐K‐8644, or K+ depolarization which activates voltage‐sensitive Ca2+ channels). In order to test whether all effects of dopamine and somatostatin were mediated by inhibitory guanosine triphosphate binding proteins, the experiments were systematically carried out in the presence or absence of pertussis toxin, an agent which selectively uncouples given subsets of G proteins from corresponding receptors.Dopamine markedly inhibited basal as well as thyrotropin‐releasing hormone‐, vasoactive intestinal peptide‐, forskolin‐ and BAY‐K‐8644‐stimulated release of prolactin. In contrast, dopamine was only able to induce partial inhibition of hormone release when secretion was triggered by tumour‐promoting activator, A23187 or K+ depolarization. Under all conditions tested, inhibition by somatostatin was significant, but of limited amplitude.Pertussis toxin completely reversed the effects of somatostatin. In contrast, complete reversal of dopamine effects by pertussis toxin was only achieved after hormone stimulation by tumour‐promoting activator, alone or with A23187. Under all other conditions a residual dopamine inhibition was maintained in the presence of the toxin. The amplitude of this residual toxin resistant inhibition was comparable in all other cases to that observed for unstimulated (basal) prolactin release.It is concluded that: 1) As expected, dopamine is a potent inhibitor of secretory processes involving cyclic AMP accumulation or voltage‐sensitive Ca2+ channel activation. In contrast, the amine is only a partial inhibitor of exocytosis resulting from non‐voltage‐sensitive Ca2+ channel‐gated increase in Ca2+ or direct activation of protein kinase C. 2) Somatostatin is a partial inhibitor of prolactin under all conditions tested. Dopamine and all somatostatin effects are mediated by pertussis toxin‐sensitive G proteins. However, a small, but significant, proportion of dopamine inhibition is resistant to pertussis toxin and can thus be assumed to involve a distinct mode of action. This alternate mechanism of dopamine inhibition operates under all conditions except after treatment with tumour‐promoting activator, suggesting that it can be inactivated by protein kinase C stimulation.
Effect of Exogenous Arginine Vasopressin on Adrenocorticotropin and Cortisol Release in Myotonie Dystrophy Patients: Delayed Responses of Normal Magnitude
Authors: Grice Jeffrey E. , Jackson Jane , Hewett Margot , Penfold Paula J. , Jackson Richard V. 
Published: September 2006

AbstractWe administered intramuscular arginine vasopressin (AVP) to ten normal controls and eight myotonic dystrophy patients. By measuring plasma AVP levels in five of the myotonics and all the normals, we showed that absorption and distribution of AVP was not delayed or significantly reduced in myotonics. The magnitude of the mean plasma adrenocorticotropin (ACTH) response to AVP in the myotonics was not different from that of normals, although it was significantly delayed (mean peak time, 37.5±4.9 versus 17.0 ± 3.2 min). We propose that this delay was caused by a significantly reduced ACTH secretion rate in myotonics, because the maximum rate of detection of ACTH in plasma is reduced in myotonics (0.6 ± 0.2 versus 1.7 ± 0.5 pmol/L/min), whose corticotropes, while having the same capacity to respond to the AVP stimulus, are slower to attain that capacity. The mean integrated cortisol response (AUC) was significantly smaller for myotonics (8072 ± 2017 versus 13049±1630 nmol.min/L). This may be due to the slower rate of ACTH delivery to the adrenal in myotonics. The timing of the adrenal response does not appear to be impaired in myotonic dystrophy, with the cortisol peak following the ACTH peak by approximately 15 min in both groups. The normal magnitude ACTH response to AVP in myotonics is in contrast to that seen to ACTH secretagogues acting via corticotropin‐ releasing hormone‐initiated pathways, where a rapid hypersecretion is seen. We propose a mechanism of defective calcium transport to account for these observations.
The Effect of Gonadal Steroids on Vasoactive Intestinal Peptide Concentration and Release from Mediobasal Hypothalamus and the Anterior Pituitary Gland
Authors: Lasaga Mercedes , Duvilanski Beatriz Haydee , Seilicovich Adriana , Afione Sandra , Diaz Maria del Carmen , Pisera Daniel , Traktenberg Ruth , Debeljuk Luciano 
Published: September 2006

AbstractThe effects of chronic administration of sex steroids on the content of vasoactive intestinal peptide (VIP) in the mediobasal hypothalamus and anterior pituitary were studied in adult rats.Gonadectomy had no effect on VIP concentration in the mediobasal hypothalamus or anterior pituitary gland. Estradiol benzoate (1 μg/100 g body wt/day) administered for 10 days decreased mediobasal hypothalamus VIP concentration of ovariectomized rats whereas it produced no change in mediobasal hypothalamus VIP content of orchidectomized rats. Testosterone propionate (100 μg/100 g body wt/day) administration decreased mediobasal hypothalamus VIP content in both sexes. Estradiol administration caused an increase whereas testosterone treatment resulted in a decrease in anterior pituitary VIP levels in both sexes. The effect of chronic administration of the sex steroids on VIP release from the mediobasal hypothalamus and anterior pituitary was also investigated. Estradiol increased evoked VIP release from the mediobasal hypothalamus and decreased mediobasal hypothalamus VIP content whereas testosterone decreased both mediobasal hypothalamus release and content. Chronic treatment with estradiol enhanced anterior pituitary VIP release and content while testosterone decreased both parameters studied. The data indicate that anterior pituitary VIP content is under the control of gonadal hormones and that the increased anterior pituitary VIP found after estradiol administration may be due to an augmented release from the mediobasal hypothalamus and probably an increase in anterior pituitary VIP synthesis.
Neonatal Exposure to Gonadal Hormones Affects the Development of Monoamine Systems in Rat Cortex
Authors: Stewart Jane , Kühnemann Sylvia , Rajabi Heshmat 
Published: September 2006

AbstractThe effects of neonatal gonadectomy of male, and testosterone propionate treatment of female rat pups on levels of monoamines and metabolites in the cerebral cortex were assessed using high‐performance liquid chromatography with electrochemical detection. In Experiment 1, pups were killed at 0, 4, 10 and 21 days of age and the anterior and posterior portions of cortex in each hemisphere were removed. At 21 days of age the levels of dopamine in anterior cortex were higher in males and testosterone propionate‐treated females than in females and gonadectomized males. However, dopaminergic activity developed earlier in females than in males and the gonadal hormone manipulations shifted the pattern of development to that of the other sex. In Experiment 2, the effects of these same gonadal hormone manipulations on the uptake, metabolism and storage capacity of catecholamine neurons in the cingulate, agranular insular, parietal and occipital cortex were estimated at 4 and 10 days of age by considering the difference between measured catecholamines in animals pretreated with vehicle or 2.5 mg/kg reserpine and then given 100 mg/kg L‐DOPA. Again, the data indicated earlier development of catecholamine neurons in females, especially in the agranular insular cortex. Dopamine was found to account for group differences; for when dopamine levels alone were considered it was found that, at 4 days of age, females had the highest levels in every area with the exception of the occipital cortex where gonadectomized males had equally high levels. These data suggest a mechanism that might account for sex differences in the development of specific cortical regions.
An Enkephalinergic Mechanism for the Hypothalamic Effect of Atrial Natriuretic Peptide to Inhibit Luteinizing Hormone Secretion
Authors: Huang Fong‐Lee S. , Samson Willis K. 
Published: September 2006

AbstractPrevious studies have demonstrated a hypothalamic site of action of atrial natriuretic peptide (ANP) to inhibit luteinizing hormone and an opioid mechanism has been suggested. We have identified the paraventricular nucleus as at least one locus of action of ANP since site‐specific injection of 0.1 nmol, bilaterally into this nucleus, but not the medial preoptic nuclei or arcuate nucleus, resulted in a significant inhibition of plasma levels in conscious, ovariectomized rats 90 and 120 min later. This paraventricular site of action suggested an involvement of endogenous enkephalins. The stable enkephalin analog, [D‐Pen2.5]enkephalin, when injected into the third ventricle in a dose of 1.0 nmol, produced a significant and transient inhibition of luteinizing hormone secretion similar to that seen following injection of 2.0 nmol ANP. Pretreatment of the rats 15 min before peptide injection with the selective 5 opioid antagonist naltrindole (50 μg/2 μl saline) completely prevented the luteinizing hormone‐inhibiting effects of both ANP and the enkephalin analog, δ opioid blockade failed to prevent the prolactin‐inhibiting effect of ANP but did reverse the prolactin‐stimulating effect of [D‐Pen2.5]enkephalin. Our results suggest a paraventricular nucleus site of action of ANP in addition to probable effects in the median eminence and indicate the possible enkephalinergic mediation of the peptide's ability to inhibit luteinizing hormone secretion.
In vivo Infusion of Adrenaline Stimulates Corticotropin‐Releasing Hormone‐Producing Neurons when given Centrally but not Distally
Authors: Barbanel Gérard , Ixart Guy , Assenmacher Ivan 
Published: September 2006

AbstractThere is evidence that adrenaline stimulates the release of corticotropin‐releasing hormone (CRH‐41) from hypothalamic neurons. This study was carried out to ascertain the effects of adrenaline on the perikarya and/or distal terminals of these cells. All experiments were performed on unrestrained rats having chronic intracerebroventricular cannulas in the lateral ventricle or intracerebral cannulas in the paraventricular nucleus and, additionally, a push‐pull median eminence cannula. Adrenaline (1.4 μg adrenaline bitartrate in 5 μI vehicle for intracerebroventricular infusion, or 0.7 μg in 0.25 μI for intracerebral infusion) was infused over 2 min, and 15‐min median eminence perfusate samples were collected over 2 to 3 h. In another experiment the median eminence was directly perfused for 30 min with a total of 1.2 μg (n = 4) or 12 μg (n = 3) adrenaline per rat. Intracerebroventricular or intracerebral adrenaline induced a swift, short‐lived (15 min) CRH‐41 surge which reached 7 to 10 times the basal level. Direct perfusion of the median eminence with adrenaline (around the nerve endings of CRH‐41‐producing neurons) did not stimulate CRH‐41 release and higher amine concentrations even tended to depress the neuropeptide release. The stimulatory effect of adrenaline on the corticotropic axis appears, therefore, to be restricted to the central dendro‐perikaryal region of CRH‐41‐producing neurons.
Intrahypothalamic Mu‐, not Delta‐ or Kappa‐Opioid Receptor Activation Causes Growth Hormone Secretion
Authors: Willoughby John O. , Kapoor Ranjna , Mackenzie Lorraine 
Published: September 2006

AbstractThe possible effects of opioid receptor agonists on growth hormone (GH)‐releasing factor or somatostatin neurons were examined by measuring the effects of localized intracerebral injections of mu‐, delta‐ and kappa‐selective agonists on GH secretion. Serial GH concentrations were measured in plasma in unanaesthetized male rats chronically prepared with venous and intracerebral cannulae, before and after treatment with bilateral intracerebral injections of opioid agonists in the preoptic anterior hypothalamic area and medial basal hypothalamus.In the medial basal hypothalamus, injections of the mu‐agonist DAGO (Tyr‐D‐Ala‐Gly‐(Me)Phe‐Gly‐ol) caused dose‐responsive increases in GH, the maximally effective dose being 0.001 nmoles. Injection of 10,000‐fold higher doses of the delta‐agonist DPDPE ([D‐Pen, D‐Pen]enkephalin) and the kappa‐agonist U50,488H were also effective in stimulating GH secretion. In the preoptic anterior hypothalamic area, DAGO caused dose‐responsive increases in GH, the maximally effective dose being 0.01 nmoles. U50.488H was ineffective at 1,000‐fold higher doses while DPDPE was effective at 100‐ to 1,000‐fold higher doses.We conclude that hypothalamic mu‐opioid receptor activation on or near somatostatin or GH‐releasing factor neurons causes GH secretion. Opioids capable of acting on other opioid receptors may also stimulate GH secretion, though only at doses that seem likely to affect mu‐receptors.
Oxytocin in the Bed Nucleus of the Stria Terminalis and Lateral Septum Facilitates Bursting of Hypothalamic Oxytocin Neurons in Suckled Rats
Authors: Moos F. , Ingram C. D. , Wakerley J. B. , Guerné Y. , Freund‐Mercier M. J. , Richard Ph. 
Published: September 2006

AbstractSeveral regions of the forebrain possess high densities of oxytocin (OT)‐binding sites including the bed nucleus of the stria terminalis (BST) and lateral septum (LS). In order to examine whether these regions participate in the central facilitation of the milk ejection reflex by OT, microinjections of OT (1 ng in 100 nl containing Janus Green dye) were made into the BST (13 tests) or LS (9 tests) of anaesthetized, suckled rats, while recording the electrical activity of OT neurons in the contralateral supraoptic nucleus. Histological localization of injection sites using Janus Green demonstrated that all BST injections were close to the anterior commissure, and LS injections were all located in the ventral division of the LS. Film autoradiographic visualization of OT‐binding sites (in 7 tests using [125I]OT antagonist) confirmed that the BST and LS injections were located within regions of high OT binding. Injections into both regions facilitated the milk ejection reflex by increasing either the frequency and/or amplitude of OT neuron bursts, or by triggering bursts in animals that previously had shown no milk ejection responses; the mean number of milk ejections in the 30 min before and after injection increasing from 1.6·0.5 to 3.6·0.5 for BST and from 1.5·0.6 to 3.9·0.4 for LS. The OT microinjections had a more variable effect on background activity of OT neurons, increasing firing in some cases and not in others. This facilitatory effect was similar to that induced by microinjections into the lateral ventricle, but was smaller and delayed compared to that induced by injection into the third ventricle (9 tests), possibly due to unilateral activation of target sites. The facilitatory effect was unlikely to have been due to diffusion of OT into the ventricle, since injections into control sites (striatum and thalamus) at similar distances from the ventricle (9 tests) had no facilitatory effect (number of bursts during 30 min before and after injection; 2.2·0.5 and 1.8·0.5, respectively). These data suggest that limbic structures (BST and LS) participate in the action of central OT on the pattern of milk ejections in the suckled rat.