bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Role for Vasopressin in the Stress‐Induced Inhibition of Gonadotrophin Secretion: Studies in the Brattleboro Rat
Authors: Cover P. O. , Laycock J. F. , Gartside I. B. , Buckingham J. C. 
Published: September 2006

AbstractThe effects of stress on the secretion of adrenocorticotrophin, corticosterone and luteinizing hormone (LH) in rats congenially lacking hypothalamic vasopressin (Brattleboro rats) and in normal controls of the parent strain (Long Evans) have been compared in an attempt to examine the role of vasopressin in the stress‐induced depression of gonadotrophin secretion. In the Long Evans rats, stress (0.6 mg/100g histamine, ip) initiated, within 5 and 20 min respectively, significant (P <0.01, Student's t‐test) increases in the plasma adrenocorticotrophin and corticosterone concentrations. It also caused a reduction in the serum LH concentration which was maximal at 5 min. By contrast, in the vasopressin deficient Brattleboro rats, stress had no effect on the serum LH concentration and produced only modest increases in pituitary adrenocortical activity compared with those in Long Evans controls. Pretreatment of both Long Evans and Brattleboro rats with dexamethasone (20μg/100 g ip, daily for 3 days) effectively abolished the pituitary‐adrenal response to stress. The steroid treatment also prevented the stress‐induced suppression of LH in the Long Evans rats; indeed, these animals, unlike the vehicle‐treated controls, exhibited a rise in serum LH concentration within 5 min of exposure to stress. Stress did not affect the serum LH concentrations in steroid‐treated Brattleboro rats. The results confirm previous reports that vasopressin is required for the full expression of the pituitary‐adrenocortical response stress. They also provide novel evidence which suggests that vasopressin released in stress contributes to the impairment of gonadotrophin secretion.
Neurotransmitter‐Mediated Changes in the Electrophysiological Properties of Pituicytes
Authors: Burnard Diane M. , Pittman Quentin J. , MacVicar Brian A. 
Published: September 2006

AbstractIntracellular recordings were obtained from pituicytes in the neural lobe of the isolated rat pituitary. Like other glia, pituicytes lacked action potentials in response to depolarizing current injection, but they tended to have more positive resting membrane potentials and higher input resistances than astrocytes in other preparations. Dye‐coupling typical of astrocytes was also demonstrated amongst pituicytes, and their morphologies were similar to those of pituicytes stained for glial fibrillary acidic protein. Action potentials, anode‐break spikes or barium spikes were not observed in pituicytes, even under conditions that maximized the elicitation of Ca2+‐dependent responses. This suggests that pituicytes either have no or a very low density of Ca2+ channels or Ca2+ currents that are too small to generate action potentials. Dynorphin A (1–13), a kappa‐opioid agonist, produced long‐lasting increases in pituicyte input resistance with no significant changes in resting membrane potential. Dynorphin's action was concentration‐dependent and was blocked by the opioid antagonist naloxone. This is consistent with previous reports demonstrating kappa‐opioid receptors on pituicytes in the neurohypophysis. The β‐adrenergic agonist isoproterenol (100 μM) reversed the increases in pituicyte input resistance produced by opioid application, with no significant changes in resting membrane potential. The fact that pituicytes responded to neurotransmitters suggests a functional link between pituicytes and neurosecretory nerve fibres.
Evidence that Neural Aromatization of Androgen Regulates the Expression of Sexual Behaviour in Female Musk Shrews
Authors: Rissman Emilie F. 
Published: September 2006

AbstractThe experiments reported on here were conducted to test the hypothesis that sexual behaviour in the female musk shrew (Suncus murinus) is regulated by the neural aromatization of testosterone to oestradiol. In the first experiment ovariectomized animals received subcutaneous hormone implants containing either an aromatizable androgen (testosterone or androstenedione), a non‐aromatizable androgen (dihydrotestosterone or methyltrienolone), or cholesterol. Only females that received an aromatizable androgen exhibited significant amounts of sexual behaviour as compared with controls (cholesterol). To examine the role of the oestrogen receptor, the anti‐oestrogen, tamoxifen (200 or 400 μg daily) was given to ovary intact or ovariectomized females treated with testosterone. Tamoxifen treatment had significant negative effects both on female sexual behaviour and on the weights of several peripheral tissues as compared with control treatments. A similar set of experiments was conducted to examine the effect of an anti‐androgen on female sexual behaviour. The androgen receptor blocker, flutamide, had no effect on sexual behaviour or weights of peripheral tissues. To determine whether flutamide can act as an anti‐androgen in this species two final experiments were conducted in male musk shrews. Flutamide treatment in males did affect several measures of sexual behaviour. In summary, these data demonstrate that the oestrogen receptor is involved in the control of female copulatory behaviour. The androgen receptor plays a role in the expression of male, but not female, sexual behaviour. Female musk shrews display copulatory behaviour in advance of follicular development when oestradiol concentrations in plasma are very low. Thus, they may have evolved a strategy of aromatizing peripherally produced androgens in the brain to concentrate the oestrogen required for the expression of sexual behaviour.
Effects of Ethane Dimethane Sulphonate and Orchidectomy on Luteinizing Hormone Secretion
Authors: Dong Qihan , Handelsman David J. 
Published: September 2006

AbstractThe aim of this study was to determine whether testicular products of non‐Leydig cell origin modulate rat luteinizing hormone (LH) secretion in vivo. We therefore compared the effects of ethane dimethane sulphonate (EDS), a toxin regarded as highly selective for Leydig cells, with that of bilateral orchidectomy on LH secretion in mature male Wistar rats. The intention was thereby to compare the effects of selective removal of Leydig cells with that of removing both Leydig cells and seminiferous tubules, respectively. Following a single dose of EDS (75 mg/kg, ip), plasma LH concentrations rose equally with those of castrated rats for the first 3 days. After that time, however, plasma LH concentrations in the EDS‐treated rats fell progressively below those of the orchidectomized rats despite the continuing castrate level of circulating testosterone until Day 17. The effects of EDS treatment or orchidectomy on pulsatile LH secretion were then compared after 11 days to castrate levels of testosterone. EDS‐treated rats demonstrated reduced LH pulse amplitude, mean plasma LH levels and net LH secretion compared with castrate rats, although LH pulse frequency was unaltered. However, a further group of rats treated with EDS and orchidectomized failed to demonstrate that these changes were fully reversed by the castration and therefore EDS may have direct effects upon pituitary LH secretion. In order to determine the mechanism of the reduced LH pulse amplitude after EDS treatment, a further study was conducted to determine whether EDS treatment resulted in reduced pituitary sensitivity to gonadotropin‐releasing hormone (GnRH). Responsiveness of pituitary LH to exogenous GnRH (0.01 to 10 μg/kg body wt) was studied 11 days after removal of testicular testosterone feedback by either EDS or castration. Plasma LH response was linearly related to the log of the GnRH dose. At 10 min after GnRH administration, the plasma LH response in EDS‐treated rats was less sensitive than in castrate rats. We conclude that the lesser augmentation of LH secretion between Days 3 and 17 after EDS treatment compared with castrate rats cannot be explained solely by changes in Leydig cell secretion but may involve direct effects of EDS on pituitary LH secretion or non‐Leydig cell testicular products. Dampening of LH pulse amplitude without change in LH pulse frequency together with the reduced sensitivity to GnRH in EDS‐treated rats suggests that this toxin may have direct effects on pituitary LH secretion independent of its effects on Leydig cell function.
Effects of Pentobarbital on Proopiomelanocortin Opioid Products of Neonatal Piglets During Normoxia and Hypoxia
Authors: Moss Immanuela R. , Inman Jamie D. G. 
Published: September 2006

AbstractEndogenous opioids have been shown to suppress physiological functions in the neonate. It has been suggested that anesthesia with barbiturates might enhance this suppression by influencing opioid systems directly. To explore this possibility, naive piglets, 2.2±0.8 (x̄±SD) days old, underwent one of five protocols: 1) normoxia (control); 2) 10% 02/90% N2 (hypoxia); 3) saline injection ip during normoxia (sham anesthesia); 4) pentobarbital sodium, 25 mg/kg ip, during normoxia (barbiturate anesthesia); and 5) pentobarbital sodium, 25 mg/kg ip, during hypoxia (combined hypoxia and barbiturate anesthesia). Following the inhalation of either gas mixture for at least 30 min, and precisely 30 min after an injection, blood, cerebrospinal fluid and a dorsal medullary slice containing the nucleus tractus solitarii were collected and processed for measurement by radioimmunoassay of opioid proopiomelanocortin products. These comprised β‐lipotropin (the precursor), β‐endorphin‐like immunoreactivity (containing the active peptide β‐endorphin) and N‐acetyl β‐endorphin (a deactivated peptide).The most striking result was seen in the cerebrospinal fluid: As compared to barbiturate anesthesia, peptide levels with all other treatments, including combined hypoxia and barbiturate anesthesia, were consistently higher. In the plasma, peptide levels after either combined hypoxia and barbiturate anesthesia or hypoxia alone were generally higher than those of their respective controls (sham anesthesia, control). Plasma levels of β‐endorphin‐like immunoreactivity and estimated β‐endorphin with combined hypoxia and barbiturate anesthesia were also higher than those with barbiturate anesthesia. The latter pattern was reversed in the nucleus tractus solitarii, in which β‐endorphin‐like immunoreactivity and estimated β‐endorphin levels were lower with combined hypoxia and barbiturate anesthesia than with barbiturate anesthesia alone, although no significant differences were achieved.These results suggest that pentobarbital may decrease the central neuronal release of active endorphins, and thus decrease the quantity of these ligands available for interaction with opioid receptors. Hypoxia, on the other hand, appears to increase such release even in the presence of pentobarbital. Thus, during a hypoxic insult, the suppressive influence of opioids on physiological functions would be enhanced regardless of the presence of barbiturate anesthesia.
Regulation of Melatonin Release and N‐Acetyltransferase Activity in Ovine Pineal Cells
Authors: Van Camp Gilles , Ravault Jean‐Paul , Falcón Jacky , Collin Jean‐Pierre , Voisin Pierre 
Published: September 2006

AbstractA suspension culture of ovine pineal cells was developed to investigate the regulation of melatonin synthesis and release. Dosedependent stimulation of melatonin release by a series of adrenergic agonists yielded a typical β‐adrenergic profile. Serotonin N‐acetyltransferase (NAT), the rate‐limiting enzyme in melatonin biosynthesis, was also stimulated by a β‐adrenergic mechanism. However, NAT activity appeared less sensitive than melatonin release to β‐adrenergic stimulation. No evidence was obtained for a contribution of α1‐adrenergic receptors to the regulation of NAT activity and melatonin release. Activation of adenylate cyclase by forskolin or addition of a cyclic AMP analogue increased both melatonin release and NAT activity. In contrast, the Ca2+ ionophore A23187 stimulated melatonin release without a detectable increase in NAT activity. Together, the present data argue for a β‐adrenergic regulation of both NAT activity and melatonin release in ovine pinealocytes. The evidence also suggests that two intracellular mechanisms may control melatonin release in ovine pinealocytes: a cyclic AMP‐dependent mechanism, associated with an increase in NAT activity and a Ca2+‐dependent mechanism, independent of NAT activity.
Effects of Various Types of Hypothalamic Deafferentation on Luteinizing Hormone Pulses in Ovariectomized Rats
Authors: Ohkura Satoshi , Tsukamura Hiroko , Maeda Kei‐ichiro 
Published: September 2006

AbstractThe pulsatile luteinizing hormone (LH) secretion in chronically ovariectomized rats bearing various types of hypothalamic deafferentation was examined. Ovariectomized rats were subjected to complete, anterolateral or anterior hypothalamic deafferentation and bled every 6 min for 3 h through an indwelling atrial cannula 5 days after the brain surgery. Another group of ovariectomized animals was subjected to posterior‐anterior hypothalamic deafferentation (PAD), which cut off the anterior part of the arcuate nucleus from the mediobasal hypothalamus, and bled 1, 3 or 5 weeks after the deafferentation. Coronal sections of the brain were immunostained with anti‐LH‐releasing hormone (LHRH) serum. The pulsatile LH secretion was observed in rats bearing anterior, anterolateral or complete hypothalamic deafferentation and these types of deafferentation did not affect the frequency of LH pulses. The mean LH level during the 3‐h sampling period and the amplitude of LH pulses decreased as the incision extended postero‐laterally. Rats bearing PAD showed an irregular fluctuating pattern in plasma LH concentration 1 week after PAD. Parameters of LH pulses were restored with time after PAD. This suggests that the system generating LHRH pulses severed by PAD had been reorganized. LHRH‐immunopositive neuronal fibres were found in the external layer of the median eminence in the rats bearing any type of deafferentation. The present results suggest that the frequency of LH pulses could be controlled by the LHRH pulse generator, which consists of non‐LHRH neurons and is located in the mediobasal hypothalamus.
Phospholipase A2 and Somatostatin Release are Activated in Response to N‐Methyl‐D‐Aspartate Receptor Stimulation in Hypothalamic Neurons in Primary Culture
Authors: Rage Florence , Pin Jean‐Philippe , Tapia‐Arancibia Lucia 
Published: September 2006

AbstractWe have recently shown that glutamate primarily induces somatostatin release in hypothalamic neurons through N‐methyl‐D‐aspartate (NMDA)‐type receptor sites. Here we report that glutamate and NMDA also stimulate the release of [3H]arachidonic acid in a dose‐dependent manner. The NMDA‐induced effects (arachidonic acid release and somatostatin secretion) were both inhibited by MK‐801, an NMDA receptor‐type antagonist, or mepacrine, a phospholipase A2 inhibitor. In addition, mepacrine was able to inhibit A23187‐stimulated arachidonic acid release and somatostatin secretion. p‐Bromophenacylbromide, another phospholipase A2 inhibitor, also blocked NMDA‐induced secretion of somatostatin. However, responses to NMDA were unaffected by H7 (inhibitor of protein kinase C), nordihydroguaiaretic acid or indomethacin (inhibitors of lipoxygenase and cyclooxygenase). Melittin, a phospholipase A2 activator, was found to stimulate both responses, but omission of extracellular Ca2+ from the incubation media strongly reduced melittin‐induced somatostatin release. Six‐h pertussis toxin pretreatment did not significantly reduce the action of NMDA on either of the two parameters studied. High‐performance liquid chromatography analysis of [3H]metabolites released in the medium after NMDA stimulation revealed that [3H]arachidonic acid was the only detectable metabolite. External addition of arachidonic acid increased the release of somatostatin, whereas E2 and F2α prostaglandins had no effect. Our results show a close correlation between arachidonic acid release and somatostatin secretion, the two parameters we investigated.
Inhibitory Actions of Acute Estradiol Treatment on the Activity and Quantity of Tyrosine Hydroxylase in the Median Eminence of Ovariectomized Rats
Authors: Pasqualini Catherine , Leviel Vincent , Guibert Bernard , Faucon‐Biguet Nicole , Kerdelhué Bernard 
Published: September 2006

AbstractThe effects of acute estradiol (E2) treatment on both the activity of tyrosine hydroxylase (TH) in the median eminence and the serum level of prolactin (PRL) were investigated. Twelve‐day‐ovariectomized rats were injected with 17β‐E2 (25μg sc) at 1100 h and sacrificed hourly from 1200 to 2300 h. TH activity was quantified by measuring the amount of exogenous tyrosine converted to L‐DOPA in vitro by aliquots of median eminence homogenates. Serum PRL levels were evaluated by radioimmunoassay. A biphasic response of TH activity to treatment was observed: an immediate decrease occurred—preceding and accompanying a rise in serum PRL—followed by an increase beyond control levels 2 h after the maximal release of PRL. The increase in TH activity could be prevented by the pretreatment of rats with a specific rat PRL antiserum, suggesting it was not due to E2 per se but rather mediated by the E2‐induced PRL elevation. To pin‐point the process underlying the E2‐induced decrease in TH activity, we evaluated the kinetic parameters of TH in the median eminence as well as its quantity (by Western blot analysis) in the median eminence and arcuate nucleus. Finally, we used a sensitive dot‐blot assay to quantify specific TH messenger ribonucleic acid in the arcuate nucleus. The decrease in TH activity after E2 treatment paralleled an immediate decrease in the affinity of TH for its pterin cofactor (6‐MPH4), while Vmax remained unchanged. A decrease in the amount of TH protein in the arcuate nucleus and median eminence as well as in the TH messenger ribonucleic acid level in the arcuate nucleus was also observed, but the latency of these effects precluded a major involvement in the immediate decline of TH activity. Therefore, when observed separately from those of PRL, E2 effects on TH in tuberoinfundibular dopaminergic neurons are clearly inhibitory consisting of a ‘deactivation’ of the enzyme together with a reduction of its synthesis.
Stimulation of Luteinizing Hormone‐Beta Messenger Ribonucleic Acid and Post‐Translational Modification of Luteinizing Hormone Isoforms by Second Messengers Mediating the Action of Gonadotrophin‐Releasing Hormone
Authors: Leigh A. J. , Wilson C. A. , Edger M. J. , Tipping K. E. , Patel M. , Chapman A. J. , Whitehead S. A. 
Published: September 2006

AbstractSeveral second messenger systems have been implicated in mediating the action of gonadotrophin‐releasing hormone on the pituitary gonadotrophs and numerous studies have shown that activation of these systems induces luteinizing hormone (LH) secretion. However, it is not known how gonadotrophin‐releasing hormone or the second messenger systems induce de novo LH biosynthesis and post‐translational modification of the hormone. In these experiments hemipituitary glands have been perifused with drugs which activate second messengers or stimulate protein kinase C directly. The LH secretory responses have been correlated with measurements of common a and LHβ mRNA and the molecular species of LH which were present in the pituitary perifusate after exposure to the drugs.Gonadotrophin‐releasing hormone (50 ng/ml, 42 nM), with and without the presence of extracellular Ca2+, the Ca2+ ionophore, A23187 (10 μM), and phorbol 12‐myristate (1 μM) all stimulated an increase in LHβ mRNA compared with controls and the appearance of a different isoform of LH to that found stored in and released from the unstimulated pituitary gland. Phospholipase C was without effect on LHβ mRNA levels and showed minimal efficacy in inducing the appearance of the different LH isoform.
Autoradiographic Detection of Oxytocin‐ and Vasopressin‐Binding Sites in Various Subnuclei of the Bed Nucleus of the Stria Terminalis in the Rat. Effects of Functional and Experimental Sexual Steroid Variations
Authors: Kremarik P. , Freund‐Mercier M. J. , Stoeckel M. E. 
Published: September 2006

AbstractOxytocin‐ and vasopressin‐binding sites were detected by autoradiography on films and on emulsion‐coated sections of rat brains using highly selective [125|]‐labelled oxytocin and vasopressin antagonists. Two distinct areas with high concentrations of oxytocin‐binding sites were detected in the bed nucleus of the stria terminalis: 1) the principal encapsulated nucleus and the associated cell‐sparse zone in the posterior medial part, and 2) the oval nucleus in the anterior lateral part. A weak diffuse labelling was, in addition, detected around the oval nucleus in the anterior lateral and anterior dorsal areas. The vasopressin‐binding sites were restricted to the anterior lateral part of the bed nucleus of the stria terminalis where they were highly concentrated in the juxtacapsular nucleus and present with lower density in a discrete cell group dorsal to the oval nucleus.Autoradiographic analyses of the bed nucleus of the stria terminalis from pregnant, lactating and ovariectomized rats (oestradiol treated or not) indicated that only the oxytocin‐binding sites in the principal encapsulated nucleus and the associated cell‐sparse zone were oestrogen‐dependent. These observations are in agreement with earlier data suggesting that the two major divisions of the bed nucleus of the stria terminalis are involved in distinct regulations. The anterior lateral part, including the oval nucleus in which oxytocin receptors are not oestrogen‐dependent, is, rather, involved in central autonomie regulations. The posterior medial part, where oestrogen‐dependent oxytocin receptors are concentrated in the principal encapsulated nucleus and the associated cell‐sparse zone, is implicated in neuroendocrine regulations and in reproductive behaviour.