bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inhibition of Sexual Maturation in Male Rats by Melatonin: Evidence Linking the Mechanism of Action to Changes in the Regulation of Hypothalamic Neuropeptide Y
Authors: Corder Roger , Walker C. Dominique , Gaillard Rolf G. , Aubert Michel L. 
Published: September 2006

AbstractActivation of gonadotrophin‐releasing hormone (GnRHJ pathways is a pivotal event in the process of sexual maturation, however the regulatory influences that precipitate this change and lead to the onset of puberty remain poorly understood. Recent studies indicate that neuropeptide Y (NPY) may participate in the regulation of luteinizing hormone secretion by modulating the pattern of GnRH secretion and by directly altering the pituitary responsiveness to GnRH stimulation. To determine whether NPY plays a role in puberty‐associated changes in hypothalamic function, levels of NPY‐like immunoreactivity (NPY‐IR) were measured in a fragment of the hypothalamus encompassing the median eminence and medial portion of the arcuate nucleus (ME‐AN), and also in the remainder of the hypothalamus from male rats of different ages. To identify changes in hypothaiamic NPY linked to the process of sexual development, the effect of delaying sexual maturation by daily afternoon administration of 100 μg melatonin (MT) from 20 to 40 days was investigated. In the hypothalamus and ME‐AN, total NPY content increased progressively with age. Expressed as a concentration (fmol/μg extracted protein), peak values for the ME‐AN (55.4 ± 7.0) were observed at 30 days of age followed by a decline to lower levels (30.2 ± 1.9) at 40 days. Daily afternoon administration of MT from 20 days of age resulted in significant increases (P<0.01) in the levels of NPY‐IR in the ME‐AN compared to control values at 30 and 40 days of age. MT was without effect on NPY‐IR levels in the remainder of the hypothalamus. When MT was administered in the early morning, a procedure which does not delay sexual maturation, NPY‐IR values for the ME‐AN region were not different from control rats indicating that the MT‐induced changes in NPY were related to the effects on sexual maturation. Using pituitary luteinizing hormone content and seminal vesicle weight as indices of sexual development, significant inverse correlation coefficients (P<0.001) between these parameters and the NPY concentration in the ME‐AN were observed (r =−0.79 and −0.70, respectively). From published data it is not possible to conclude whether the main effects of NPY are exerted at the hypothalamic or pituitary level. However, the changes in the NPY content of the ME‐AN observed during the onset of puberty, and the influence of MT on these changes, support assertions that NPY is involved in the regulation of sexual maturation.
Inhibition of Prolactin Release by Gonadotropin‐Releasing Hormone‐Associated Peptide in Benign, Dopamine‐Sensitive and in Malignant, Dopamine‐Resistant Pituitary Tumors
Authors: Forget Hélèns , Lafond Julie , Collu Robert 
Published: September 2006

AbstractSince the gonadotropin‐releasing hormone‐associated peptide (GAP) has been reported to be capable of inhibiting prolactin release from normal lactotrophs, with the present study we have examined the in vitro effects of GAP on prolactin release in an estrone‐induced, dopamine‐sensitive rat pituitary adenoma and two malignant, transplantable and dopamine‐resistant rat pituitary tumors, 7315a and MtTW15. Enzymatically dispersed cells obtained from the three types of tumor were cultured in multiwell dishes for 4 days. On the fifth day, the cells were exposed for 4 h to human GAP 1–56 or to the analog GAP 42–56 or to rat GAP 1–53, at various concentrations. In some experiments, the effect of a pretreatment of the cells for 16 h with pertussis toxin before exposure to human GAP was also evaluated. In the three tissues, rat GAP was able to inhibit prolactin release in a dose‐dependent manner. Human GAP 1–56 and GAP 42–56 were able to inhibit prolactin release in a dose‐dependent manner in all cells except those of the MtTW15 tumor. Furthermore, in adenomatous cells, the inhibitory effects of these peptides were suppressed by pretreatment of the cells with pertussis toxin. These findings indicate that GAP is capable of inhibiting prolactin release even in dopamine‐resistant pituitary tumors. This inhibition is exerted through a pertussis toxin‐sensitive G‐protein‐dependent signaling mechanism in adenomatous cells.
Cellular Levels of Messenger Ribonucleic Acids Encoding Vasoactive Intestinal Peptide and Gastrin‐Releasing Peptide in Neurons of the Suprachiasmatic Nucleus Exhibit Distinct 24‐Hour Rhythms
Authors: Zoeller R. Thomas , Broyles Brad , Earley John , Anderson Earl R. , Alberst H. Elliott 
Published: September 2006

AbstractThere is strong evidence supporting the view that the Suprachiasmatic nucleus (SCN) functions as a circadian clock; however, the neural and molecular events underlying SCN function remain unclear. A specific subpopulation of neurons within the ventrolateral aspect of the SCN that contains three peptides, vasoactive intestinal peptide (VIP), peptide histidine isoleucine (PHI) and gastrin‐releasing peptide (GRP), play an important role in SCN function. VIP‐containing neurons of the SCN receive synapses from photic projections, and co‐injection of all three peptides mimics the phase‐delaying effects of light on circadian activity rhythms. In principle, the signaling potential of a neuron containing several transmitters may be affected by the concentration ratio of co‐released factors; hence, one mechanism by which VIP/PHI/GRP‐containing neurons could influence SCN function is by changing the concentration ratio of these peptides throughout the light‐dark cycle. The present study was performed to examine this possibility. Relative cellular levels of mRNA encoding both VIP/PHI and GRP were determined within the SCN every 4 h in rats housed in a 14 h light: 10 h dark cycle. Quantitative in situ hybridization revealed a statistically significant (P<0.005) 24‐h profile of changes in VIP/PHI mRNA that peaked during the dark phase, and a significant (P<0.005) 24‐h profile of changes in GRP mRNA that peaked during the light phase. These data support the interpretation that cellular levels of mRNAs encoding VIP/PHI and GRP within the SCN exhibit distinct profiles of changes throughout the light‐dark cycle. Further, these findings are consistent with the hypothesis that the concentration ratio of VIP and PHI to GRP changes over the light‐dark cycle, and that this may be an important mechanism by which circadian rhythms are generated or entrained.
Ovariectomy Increases in vivo Luteinizing Hormone‐Releasing Hormone Release in Pubertal, but not Prepubertal, Female Rhesus Monkeys
Authors: Chongthammakun Sukumal , Claypool Lee E. , Terasawa Ei 
Published: September 2006

AbstractIn pubertal, but not prepubertal, monkeys ovariectomy (OVX) results in an elevation of circulating luteinizing hormone (LH) levels. To determine if the castration‐induced LH increase in pubertal monkeys is due to an increase in pulsatile LH‐releasing hormone (LHRH) release, effects of OVX on in vivo LHRH release in the stalk‐median eminence were examined in fully conscious monkeys using a push‐pull perfusion method. The average ages (± SEM) of female rhesus monkeys in each group at OVX were 14.5±0.6 months (n = 6; prepubertal), 25.0±1.3 months (n = 5; early pubertal) and 37.8 ± 2.1 months (n = 6; midpubertal). Perfusate samples from the stalk‐median eminence were obtained in 10‐min fractions for 6 h in the morning (0600 to 1200 h) and 6 h in the evening (1800 to 2400 h), from the same subjects before OVX, and at 29 days and approximately 100 days after OVX. LHRH levels in perfusates were measured by radioimmunoassay. LH levels throughout the experiment were monitored by periodic blood sampling.OVX resulted in a significant LH increase in early and midpubertal monkeys (P> 0.001 for both), but not in prepubertal monkeys. Similarly, OVX in early and midpubertal monkeys increased mean LHRH release when examined 29 days after surgery (P> 0.05 and P> 0.01, respectively). The OVX‐induced LHRH increases in early and midpubertal monkeys remained elevated at approximately 100 days postcastration. Furthermore, it was found that effects of OVX on the increased LHRH release were primarily due to the elevation of basal release and pulse amplitude, but not pulse frequency. In contrast, OVX did not cause any significant effects on pulsatile LHRH release in prepubertal monkeys.The results indicate that an increase in LHRH release and a concomitant increase in circulating LH occurs after OVX in pubertal monkeys, but not in prepubertal monkeys. These data are consistent with the hypothesis that the low level of LH in circulation before the onset of puberty is due to a low amount of LHRH release which is independent of ovarian steroid feedback and that the maturity of the neuronal control system for the pulsatile LHRH release is responsible for the onset of puberty. After the onset of puberty, the negative feedback of ovarian steroid hormones becomes important to the regulation of gonadotropin release.
Acetyl‐L‐Carnitine Effect on Pituitary and Plasma β‐Endorphin Responsiveness to Different Chronic Intermittent Stressors
Authors: Bidzinska Bozena , Petraglia Felice , Angioni Stefano , Genazzani Alessandro D. , Criscuoio Mario , Ficarra Guido , Gallinelli Andrea , Trentini Gian Paolo , Genazzani Andrea R. 
Published: September 2006

AbstractThe aims of the present study were: 1) to compare the effect of two different chronic intermittent stressors i.e. cold‐swimming versus ether, on the pituitary opioidergic system; 2) to evaluate the response of pituitary and plasma β‐endorphin (βS‐EP) to an acute stress in chronically stressed rats; and 3) to evaluate the effect of acetyl‐l‐carnitine treatment (10 mg/day/rat per os at night) on pituitary and plasma β‐EP changes induced by two different types of chronic stress. The stressors were applied twice a day for 10 days. Rats were killed either before, during or after the last swimming or ether stress session. β‐EP was measured by radioimmunoassay in anterior pituitary and in neurointermediate lobe extracts and in plasma. The following observations were made; 1) Chronic intermittent cold‐swimming stress increased anterior pituitary contents and plasma β‐EP levels; 2) both chronic intermittent cold‐swimming stress and ether stress caused an increase of neurointermediate lobe β‐EP contents; 3) as in control animals, rats exposed to chronic intermittent swimming stress reduced pituitary β‐EP contents and raised plasma β‐EP levels in response to the last acute swimming stress; 4) in contrast to control animals, rats exposed to chronic intermittent ether stress did not show any significant response of the pituitary‐plasma opioidergic system to the last acute ether session; 5) the acetyl‐l‐carnitine treatment counteracted the changes evoked by chronic intermittent cold‐swimming stress on the pituitary and plasma β‐EP levels. The present data show that chronic intermittent ether stress impairs the capacity to respond to the acute stress and that acetyl‐l‐carnitine may modulate the changes of β‐EP levels following chronic cold‐swimming stress exposure.
Corticotropin‐Releasing Hormone Neurons in the Paraventricular Nucleus Project to the External Zone of the Median Eminence: A Study Combining Retrograde Labeling with Immunocytochemistry
Authors: Lennard David E. , Eckert William A. , Merchenthaler Istvan 
Published: September 2006

AbstractCorticotropin‐releasing hormone (CRH) is the major regulator of the pituitary‐adrenal axis. CRH‐immunoreactive perikarya are widely distributed in the central nervous system; however, only those which participate directly in the regulation of adrenocorticotropin are connected to the portal circulation in the external zone of the median eminence. The present study describes the identification of these hypophysiotropic neurons using retrograde labeling and CRH immunocytochemistry. Fuoro‐Gold was injected peripherally then, 5 days later, the animals were treated with colchicine. Twenty‐four hours later the animals were sacrificed, and their brains were immunostained for CRH with the indirect immunofluorescence technique. The results indicate that the vast majority of the Fluoro‐Gold‐accumulating and CRH‐immunopositive perikarya (hypophysiotropic neurons) are located in the medial parvicellular subdivision of the paraventricular nucleus (PVN). However, not each CRH‐immunoreactive neuron contains Fluoro‐Gold, i.e. a small portion of these neurons project to areas of the brain other than the median eminence. The anterior, lateral and periventricular subdivisions of the PVN also contain hypophysiotropic CRH‐immunoreactive perikarya, however, their number is much less than in the medial parvicellular subdivision. Scattered double‐labeled cells are also present in the medial preoptic area and the dorsal hypothalamus, just behind the PVN. These results support previous observations that the PVN, particularly the medial parvicellular subdivision, is the predominant source of the hypophysiotropic CRH neurons.
α2 and β Adrenoceptors in the Mediobasal Hypothalamus and α2 Adrenoceptors in the Preoptic‐Anterior Hypothalamus Stimulate Prolactin Secretion in the Conscious Male Rat
Authors: Kapoor Ranjna , Chapman Ian M. , Willoughby John O. 
Published: September 2006

AbstractPlasma prolactin concentrations were measured in unanaesthetized male rats before and after stereotaxic microinjection of adrenergic agents into the mediobasal and preoptic‐anterior hypothalamus.In the mediobasal hypothalamus injection of the α2 agonist clonidine produced a dose‐dependent increase in prolactin secretion over the dose range 0.1 to 10 nmoles, the stimulation due to 1 nmole being blocked by idazoxan (α2 antagonist). Stimulation of prolactin release was also caused by isoprenaline (β agonist) and was significantly reduced by the β antagonist propranolol. The β2 agonist salbutamol was also effective in stimulating prolactin secretion. However, the adrenergic agonists, noradrenaline (mixed α and β), phenylephrine (α1) and tyramine (sympathomimetic) failed to affect prolactin secretion.In the preoptic‐anterior hypothalamus clonidine caused a dose‐dependent increase in prolactin secretion over the dose range 0.001 to 10 nmoles, the stimulation due to 0.1 nmole being abolished by idazoxan. While prolactin levels were significantly elevated by noradrenaline and tyramine, phenylephrine was ineffective.We conclude that the activation of α2 and β2 adrenoceptors in the mediobasal hypothalamus and of α2 adrenoceptors in the preoptic‐anterior hypothalamus, on or near prolactin‐regulating neurons, results in increased prolactin secretion. An α1 inhibitory action in the mediobasal hypothalamus has however not been ruled out. Adrenergic inputs in the preoptic‐anterior hypothalamus appear to exert a predominant facilitatory effect on prolactin secretion.
Radioimmunocytochemical Distribution of Neutral Endopeptidase (Enkephalinase E.G.3.4.24.11) at the Ultrastructural Level in the Rat Median Eminence
Authors: Vandenbulcke Franck , Pollard Hélène , Mitchell Valérie , Beauvillain Jean‐Claude 
Published: September 2006

AbstractNeutral endopeptidase (E.G. 3.4.24.11) was visualized at the ultrastructural level in the external zone of the rat median eminence by using 125|‐labelled IgG of a monoclonal serum.A precise analysis of the localization of the immunolabelling, which appears in the form of individual stray silver grains, was undertaken. Among the 1,045 grains counted, 82% were localized over membrane appositions involving nerve endings only and nerve endings plus tanycytes. The difference between the real and a randomly generated population of grains was statistically significant. Our results provide morphological arguments in support of the view of a paracrine action of neuropeptides present in the median eminence especially enkephalins but possibly, substance P, angiotensin, cholecystokinin and neurotensin. These neuropeptides are known to be inactivated by neutral endopeptidase. The action of these peptides may be exerted on nerve endings (autocrine or paracrine) but an intervention on tanycytes cannot be excluded.
Melatonin and the Circadian Clock in Mink: Effects of Daily Injections of Melatonin on Circadian Rhythm of Locomotor Activity and Autoradiographic Localization of Melatonin Binding Sites
Authors: Bonnefond Catherine , Monnerie Régine , Richard Jean‐Pierre , Martinet Lise 
Published: September 2006

AbstractThe present study examines a putative effect of exogenous melatonin on the Circadian organization of the mink. Two approaches were used to determine first whether entrainment of free‐running rhythms of locomotor activity in constant darkness can be obtained by daily melatonin injections, thus demonstrating a control of melatonin on the clock generating Circadian rhythms, the suprachiasmatic nucleus of the hypothalamus. Entrainment was never obtained in the 8 vehicle‐injected females and 7 out of the 8 melatonin injected‐ones. In 3 females free‐running in constant darkness, a phase advance followed by a few days of transient effect was observed when melatonin injections coincided with the onset of activity. However, the comparison of the regression of the daily activity onset related to successive days by covariance analysis revealed that true entrainment was effective in only 1 female. Second, we examined the distribution of melatonin binding sites within the brain of juvenile and adult mink using an in vitro autoradiographic procedure with [125l]2‐iodomelatonin. No binding sites were observed in the suprachiasmatic nucleus of any of the animals. However, all animals displayed a high density of melatonin binding sites in the pars tuberalis of the pituitary. The relation between a modulatory control of melatonin on the Circadian clock and the presence and density of melatonin binding sites in the clock is discussed. In mink, melatonin does not seem to act as an internal Zeitgeber.
Sex and Species Differences in the Vasopressin Innervation of Sexually Naive and Parental Prairie Voles, Microtusochrogasterand Meadow Voles,Microtus pennsylvanicus
Authors: Bamshad Maryam , Novak Melinda A. , De Vries Geert J. 
Published: September 2006

AbstractTo study whether central systems that are implicated in functions associated with reproduction show different changes in males and females that become parental, the central vasopressin (AVP) innervation was compared in two species of voles: prairie voles, in which males and females provide parental care, and meadow voles, in which only females provide parental care. For both species, the densities of AVP‐immunoreactive (AVP‐ir) fibers in the lateral septum, lateral habenular nucleus, medial preoptic area and paraventricular nucleus of the thalamus were compared in males and females that were sexually inexperienced or had become parents 6 days before sacrifice. The lateral septum and lateral habenular nucleus presumably receive their projections from the bed nucleus of the stria terminalis and medial amygdaloid nucleus, while the other two areas presumably receive their projections from the suprachiasmatic nucleus. Differences between sexually naive and parental animals were found only in the presumed projections of the bed nucleus of the stria terminalis and medial amygdaloid nucleus. In both species, AVP‐ir fiber densities in the lateral habenular nucleus and the lateral septum were much greater in males than in females regardless of parental state. In prairie voles, AVP‐ir fiber density in the lateral septum and lateral habenular nucleus was reduced in parental males, while no differences were found in females. In parental meadow voles, the AVP‐ir fiber density in the lateral septum did not show changes, while the fiber density in the lateral habenular nucleus was increased. The reduction in AVP‐ir fiber density in parental prairie vole males and the absence of such a reduction in meadow vole males may be related to differences in their contribution to parental care.
Endogenous Opioid Regulation of Oxytocin Secretion Through Pregnancy in the Rat
Authors: Douglas A. J. , Dye S. , Leng G. , Russell J. A. , Bicknell R. J. 
Published: September 2006

AbstractWe have investigated the influence of endogenous opioids on oxytocin secretion during pregnancy. In blood‐sampled consciousrats on days 18 and 21 of pregnancy plasma oxytocin concentration, measured by radioimmunoassay, was significantly increased compared to non‐pregnant or post‐partum rats. On days 15, 18 and 21 of pregnancy, but not in non‐pregnant, early pregnant or post‐partum rats, the opioid antagonist naloxone caused a significant increase in plasma oxytocin compared to vehicle injection, indicating activation of an endogenous opioid restraint over oxytocin secretion.Electrically stimulated neural lobes isolated from 16‐ and 21‐day pregnant rats released more oxytocin than those from non‐pregnant rats. However, naloxone (10−5 M) was less effective at potentiating, and the k‐opioid agonist U50,488 (10−5 M) was less effective at inhibiting, stimulated release at the end of pregnancy than in non‐pregnant rats suggesting desensitization of oxytocin nerve terminals to actions of endogenous opioids. Neural lobes from male rats drinking 2% saline for 4 days also showed desensitization of oxytocin nerve endings to naloxone.Neither neural lobe content of dynorphin A(1–8), an endogenous k‐opioid, nor prodynorphin mRNA expression, measured by in situ hybridization histochemistry in the supraoptic nucleus altered during pregnancy. However, neural lobe content of Met5enkephalin significantly decreased by day 21 of gestation suggesting enhanced release. We conclude that an endogenous opioid, possibly a product of proenkephalin A in oxytocin cells may be responsible for auto‐inhibition of oxytocin release during gestation, and that this mechanism desensitizes in late pregnancy at a time when other opioid inputs to the oxytocin neurons become activated to provide an overall increase in opioid restraint of the system. The changes in opioid input through pregnancy may be involved in initiation and regulation of oxytocin secretion at parturition. A similar opioid mechanism, but possibly involving dynorphin, could explain desensitization in saline drinking rats and indicates that desensitization may be a consequence of chronic activation of secretion from the oxytocin nerve terminals rather than a phenomenon peculiar to pregnancy.