bluuebunny/crossref_metadata_2025_split huggingface dataset:
Changes in Feeding Activity, Plasma Luteinizing Hormone, and Testes Weight in Ring Doves Following Hypothalamic Injections of Prolactin
Authors: Foreman Kenneth T. , Lea Robert W. , Buntin John P. 
Published: September 2006

AbstractMicroinjections of ovine prolactin were administered unilaterally to the ventromedial hypothalamic nucleus and the preoptic‐suprachiasmatic region in adult male ring doves in an attempt to determine the site(s) at which intracranial injections of prolactin act to alter feeding behaviour and gonadotropin secretion in this species. Food intake and body weight were measured daily during a 6‐day pretreatment period and the 5‐day treatment period that immediately followed. During the treatment period, birds received twice daily injections (0.5 μl) of either 2.5 ng ovine prolactin or saline vehicle. An additional group of birds with cannulae in the ventromedial nucleus were given twice daily injections of 25 ng ovine prolactin. Although food consumption was unaffected by low dose prolactin treatment, birds given 25 ng prolactin injections into the ventromedial nucleus showed a significant augmentation in food intake. Injections of 25 ng prolactin into the preoptic area also increased feeding; however, the magnitude of this hyperphagic response, as expressed relative to pretreatment levels, was less than that observed following prolactin injection into the ventromedial nucleus. No differences were observed between prolactin‐treated and vehicle‐treated birds in either cannulation group when testes weights and plasma luteinizing hormone concentrations were compared at the end of the treatment period. However, the possibility that prolactin influenced changes in luteinizing hormone and testes weight relative to baseline values could not be assessed due to constraints imposed by the experimental paradigm used. These results suggest that prolactin‐sensitive neurons in the ventromedial hypothalamic region and the preoptic area are potential sites of prolactin action in promoting hyperphagia in ring doves. However, the role of these sites in mediating prolactin‐induced suppression of gonadotropin secretion in this species remains to be clarified.
Castration Reduces the Nocturnal Rise of Pineal Melatonin Levels in the Male Rat by Impairing its Noradrenergic Input
Authors: Hernandez G. , Abreu P. , Alonso R. , Santana C. , Moujir F. , Calzadilla C. H. 
Published: September 2006

AbstractThe effects of castration and testosterone treatment on pineal day‐night rhythms were studied in male rats. Bilateral gonadectomy was performed at 21 days of age. Testosterone propionate was given subcutaneously to castrated animals in a dose of 10 μg/100 g body weight during two consecutive days before sacrifice. Animals were killed 40 days after gonadectomy at four different times of a 12:12 h light‐dark cycle (1600, 2400, 0400 and 0800h). Tyrosine hydroxylase activity was measured in individual pineals by means of high‐performance liquid chromatography determination of L‐DOPA formed. Pineal levels of norepinephrine, dopamine, 5‐hydroxytryptamine and 5‐hydroxyindole acetic acid were determined by high‐performance liquid chromatography with amperometric detection, while pineal melatonin content was measured by radioimmunoassay. Castration abolished the day‐night rhythms of pineal tyrosine hydroxylase activity and norepinephrine content, both by elevating their daytime levels and by blocking their nocturnal rise. In addition, gonadectomy drastically modified pineal indoleamine metabolism by increasing daytime levels of both 5‐hydroxytryptamine and 5‐hydroxyindole acetic acid, and by reducing the nocturnal elevation of pineal melatonin content. Testosterone treatment was unable to prevent the effect of orchidectomy on pineal rhythms of tyrosine hydroxylase activity, 5‐hydroxytryptamine or 5‐hydroxyindole acetic acid content, however it partially restored the day‐night pineal rhythms of both norepinephrine and melatonin content. These results are indicative of a possible participation of reproductive hormones in the control of pineal rhythmic activity in the male rat. Apparently, since gonadectomy abolished the nocturnal rise of both pineal tyrosine hydroxylase activity and norepinephrine content, the primary site of action of reproductive hormones could be at the level of the superior cervical ganglion.
Negative Feedback by Corticosterone is the Major Mechanism Responsible for Corticotropin‐Releasing Factor‐Induced Desensitization
Authors: Miyanaga Ken , Miyabo Susumu , Ooya Eiichi 
Published: September 2006

AbstractSubcutaneous infusion of ovine corticotropin‐releasing factor (oCRF) to male rats at a rate of 0.1 μg/h for 4 days did not alter the rise of plasma adrenocorticotropin (ACTH) and corticosterone induced by 3‐min ether exposure. In contrast, 1.0 μg/h oCRF for 4 days virtually abolished the ACTH response to ether, whereas a substantial corticosterone response was preserved. Intravenous administration of phenoxybenzamine (5 mg/kg) prior to ether stress completely inhibited the corticosterone response. Plasma ACTH and corticosterone responses in chronic CRF‐treated rats to an intravenous bolus injection of 2.0 μg oCRF were also markedly blunted by pretreatment with subcutaneous oCRF 1.0 μg/h for 4 days. Adrenalectomized rats given corticosterone in the drinking fluid at a concentration of 80 μg/ml showed a plasma corticosterone pattern mimicking the normal diurnal rhythm. Basal plasma ACTH and thymus weight were within normal limits. In these rats, the magnitude of ACTH rise to ether stress did not differ between the chronic CRF‐treated rats and the vehicle‐treated rats. In cultured pituitary cells prepared from animals infused with oCRF 1.0 μg/h for 4 days, the basal and CRF‐stimulated ACTH release was reduced by 46%. We conclude that among the possible mechanisms proposed for ‘desensitization’ during long‐term infusion of CRF, negative feedback by elevated corticosterone at both brain and pituitary levels is the primary factor. The results also suggest the existence of non‐ACTH‐mediated catecholaminergic systems in the stress‐induced adrenocortical activation.
Isolation, Amino‐Acid Sequence, Synthesis and Biological Properties of Urotensin I from Hippoglossoides elassodon
Authors: McMaster D. , Itoh H. , MacCannell K. L. , Rivier J. , Rivier C. , Vale W. , Fryer J. N. , Tran T. N. , Lederis K. 
Published: September 2006

AbstractA 41‐residue urotensin I neuropeptide (H‐UI) was isolated from urophyses of the marine teleost Hippoglossoides elassodon (the flathead sole). The peptide was recognized by its partial cross‐reactivity in a radioimmunoassay developed for Catostomus (sucker) Ul (S‐UI), and was purified by reversed‐phase high‐performance liquid chromatography. The amino‐acid sequence was shown to be H‐Ser‐Glu‐Glu‐Pro‐Pro‐Met‐Ser‐lle‐Asp‐Leu‐Thr‐Phe‐His‐Met‐Leu‐Arg‐Asn‐Met‐lle‐His‐Arg‐Ala‐Lys‐Met‐Glu‐Gly‐Glu‐Arg‐Glu‐Gln‐Ala‐Leu‐lle‐Asn‐Arg‐Asn‐Leu‐Leu‐Asp‐Glu‐Val‐NH2. H‐UI is 66% homologous with S‐UI and 63% homologous with Cyprinus (carp) Ul (C‐UI). Like S‐ and C‐UI, H‐UI is about 50% homologous with the frog skin peptide sauvagine and with Catostomus and mammalian corticotropin‐releasing factors. H‐UI had similar vasodilatory effects in mammals, and similar adrenocorticotropin‐releasing effects (in rat and goldfish) to S‐UI, C‐UI, sauvagine and the corticotropin‐releasing factors, but had relatively low potency (e.g. 10% to 30% of the vasodilatory potency of S‐ and C‐UI) in all the bioassay systems studied.
Ovarian Steroid Regulation of Pulsatile Luteinizing Hormone Release During Early Gestation in the Rat
Authors: Gallo Robert V. , Bona‐Gallo Antonella , O'Sullivan David 
Published: September 2006

AbstractThe object of this study was to examine ovarian regulation of pulsatile luteinizing hormone (LH) secretion during early gestation. This was done primarily by analyzing pulsatile LH release in rats that were either sham ovariectomized (OVX) on Day 7 of pregnancy, implanted with empty Silastic capsules, and bled on Day 8, or OVX on Day 7, immediately implanted with Silastic capsules producing plasma levels of estradiol and/or progesterone characteristic of Day 7 to 8 of pregnancy, and bled on Day 8. In addition, the role of progesterone in regulating pulsatile LH secretion was also examined by administration of the progesterone receptor antagonist, RU486, on Day 7 and examining pulsatile LH release on Day 8 of pregnancy. OVX caused a marked increase in LH pulse amplitude and frequency within 24 h. Replacement with physiological plasma levels of estradiol or progesterone alone had no suppressive effect on this OVX‐induced increase in pulsatile LH secretion. Restoration of physiological plasma levels of both estradiol and progesterone returned LH pulse amplitude to values seen in sham OVX controls, and prevented the OVX‐induced increase in LH pulse frequency. The group mean LH pulse frequency tended to be less in estradiol + progesterone‐treated rats than in sham OVX controls, but this difference was not statistically significant. RU486 blocked uterine progesterone receptors as evidenced by endometrial hemorrhaging. In agreement with the OVX + steroid replacement data, RU486 administration also resulted in increases in LH pulse amplitude and frequency. These data demonstrate that the frequency and amplitude of LH pulses on Day 8 of gestation are held in check by negative feedback signals coming from the ovary. Neither steroid alone exerts any suppressive influence over pulsatile LH secretion during early gestation, but both steroids acting together exert a prominent negative feedback regulation on the pulsatile LH release process.
Cell‐Specific Expression of the Rat Oxytocin Gene in Transgenic Mice
Authors: Young W. Scott , Reynolds Kay , Shepard Emily A. , Gainer Harold , Castel Mona 
Published: September 2006

AbstractThe genes for the posterior pituitary hormones oxytocin (OT) and vasopressin (VP) are expressed in magnocellular neurons of the hypothalamus. Previous attempts to obtain cell‐specific expression of OT and VP transgenes in mice have been unsuccessful using constructs containing only the OT or VP genes. As the endogenous genes are located near each other on the same chromosome, we investigated four transgenic mouse lines incorporating a single 5.2 k bp construct of rat genomic deoxyribonucleic acid with 1.63 k bp and 3.55 k bp of the OT and VP genes, respectively. Rat OT transcripts were detected only in transgenic mouse OT neurons of the paraventricular and supraoptic nuclei in two lines. The levels of endogenous and transgene OT transcripts increased in response to 10 days of lactation. Furthermore, rat OT‐associated neurophysin immunoreactivity was detected in magnocellular cell bodies as well as in the posterior pituitary of the transgenic but not the control mice. Cell‐specific rat VP expression was not detected in these transgenic mice.
Heterologue Conversion of Amphibian Hydrin 2 into Vasotocin Through Bovine Granule Alpha‐Amidating Enzyme
Authors: Rouillé Yves , Chauvet Jacqueline , Acher Roger 
Published: September 2006

AbstractHydrin 2 (vasotocinyl‐Gly), found along with vasotocin in the neurohypophysis of frogs and toads but not of other vasotocin‐bearers such as birds and reptiles, is believed to act on water permeability of frog skin, whereas vasotocin mainly fulfils the antidiuretic function on the kidney. In order to understand the peculiar regulation of provasotocin differential processing in amphibians, conversion of hydrin 2 into vasotocin has been attempted using bovine pituitary granule α‐amidating enzyme. Generated vasotocin has pharmacological properties and Chromatographic behaviour in high‐performance liquid chromatography identical to those of synthetic vasotocin. However, the low yield of conversion (5% to 10%) suggests that additional factor(s) might be involved in the physiological processing.
Inhibition by Brain Natriuretic Peptide of Vasopressin Neurons in the Supraoptic Nucleus and Neurons in the Region of the Anteroventral Third Ventricle in Rat Hypothalamic Slice Preparations
Authors: Yamamoto S. , Inenaga K. , Yamashita H. 
Published: September 2006

AbstractIt is not entirely clear whether or not atrial natriuretic peptide (ANP) directly inhibits vasopressin neurons in the supraoptic nucleus (SON) and paraventricular nucleus. Recently, a novel peptide, brain natriuretic peptide (BMP), which has been isolated from the brain, has been shown to have a similar action to ANP on the regulation of vasopressin release. Intracerebroventricular injection of both BNP and ANP inhibits stimulus‐evoked increases of plasma vasopressin level. The present study was undertaken: 1) to investigate whether BNP affects the activity of neurons in the region of the anteroventral third ventricle (AV3V) and SON which are involved in the control of body fluid homeostasis and blood pressure regulation, 2) to reassess effects of ANP on SON neurons, and 3) to test whether BNP exerts its effects by mechanisms which are different from those of ANP. Extracellular recordings were made from 213 AV3V and 110 SON spontaneously firing neurons in the rat coronal hypothalamic slice preparation. Of the AV3V neurons tested, BNP inhibited 86 (40%) and excited 2 (1%) while 125 neurons remained unaffected. A dose‐response relationship was obtained for 7 AV3V neurons at different BNP concentrations ranging from 10−11 M to 10−6 M; the firing rates of all 7 neurons decreased. The threshold concentration to evoke inhibitory responses was approximately 10−10M in the AV3V. When BNP and ANP were applied to the same neuron, most AV3V neurons which were inhibited by BNP were also inhibited by ANP and the neurons which were unaffected by BNP were also unaffected by ANP. Thus, these two peptides probably have a similar action on AV3V neurons. When BNP and angiotensin II were applied to a group of 60 neurons in the AV3V, most of the responsive neurons showed either inhibitory responses to BNP or excitatory responses to angiotensin II. Both BNP and ANP were applied to a group of 110 SON neurons: BNP (10 −7 M) inhibited 52 (75%) of 69 phasic (putative vasopressin) neurons, while BNP affected none of the 41 non‐phasic (putative oxytocin) neurons. By contrast, ANP inhibited only 20 (29%) of 69 phasic neurons tested but it also had no effect on 41 non‐phasic neurons tested. Our results are consistent with the suggestion that BNP is involved in the regulation of vasopressin release by acting on SON neurons and AV3V neurons.
Thyrotrophin‐Releasing Hormone Raises Cytosolic Free Calcium Concentration in Human Adenomatous Somatotrophs and Corticotrophs; Comparison with in vivo Responsiveness to Thyrotrophin‐Releasing Hormone in Patients with Acromegaly or Cushing's Disease
Authors: Spada Anna , Reza‐Elahi Farzin , Lania Andrea , Pandiella Atanasio , Bassetti Monique , Bazzoni Nicoletta , de Alamo Paloma Gil , Faglia Giovanni 
Published: September 2006

AbstractThe effect of thyrotrophin‐releasing hormone (TRH) on intracellular free Ca2+ concentration, [Ca2+)i, was investigated with the fluorescent dye fura‐2 in cell suspensions obtained from 13 human growth hormone‐secreting adenomas and 6 adrenocorticotrophin‐secreting adenomas. Preoperatively, 9 out of 13 acromegalic patients showed a positive growth hormone response to TRH administration while none of the 6 patients with Cushing's disease had a plasma adrenocorticotrophin increase after TRH injection. In all the growth hormone‐secreting adenomas the addition of TRH (100 nM) caused a significant rise in [Ca2+]i (from a resting level of 133±40 (±SD) to a value of 284±119 nM at 100 nM TRH, n = 42; P<0.001). The transient induced by TRH was found to have a dual origin, one due to Ca2+ mobilization from intracellular stores which was maintained in presence of EGTA (3mM) and verapamil (10 μM) and a plateau phase due to Ca2+ influx from the extracellular media. Somatostatin (0.1 μM) lowered both resting [Ca2+]i and TRH‐induced transients. The effect of gonadotrophin‐releasing hormone on [Ca2+]i was evaluated on cell suspensions obtained from 6 growth hormone‐secreting adenomas. Gonadotrophin‐releasing hormone (100 nM) caused a marked rise in [Ca2+]i (from 179±25 to 283±15nM) on the cell suspension obtained from the only in vivo responsive adenoma while it was ineffective in the remaining 5. Although TRH was ineffective in modifying plasma adrenocorticotrophin levels in all patients with Cushing's disease, in 5 out of 6 tumors the addition of 100 nM TRH caused a significant rise in [Ca2+]i (from 102.5 ± 36 to 163±66 nM, n = 22; P < 0.005). However, the effect of TRH on [Ca2+]i was significantly lower than that caused by arginine vasopressin, a physiological stimulator of adrenocorticotrophin release ([Ca2+]i values; 145±78 nM at 100 nM TRH versus 300±140 at 10 nM arginine vasopressin, n = 15; P<0.05). Moreover, the effect of arginine vasopressin on [Ca2+]i was detectable at concentrations as low as 0.1 nM while TRH was effective at concentrations higher than 1 nM. By contrast, gonadotrophin‐releasing hormone was ineffective in increasing [Ca2]i in all the adrenocorticotrophin‐secreting adenomas studied. Collectively, these data indicate that sensitivity to TRH is present in almost all the growth hormone‐ and adrenocorticotrophin‐secreting adenomas independently of the responsiveness of the individual patients to the peptide.
Determination of Enkephalins in Rat Cerebrospinal Fluid with High‐Performance Liquid Chromatography‐Electrochemical Detection: Increased Concentrations During Lactation are Controlled by Sucking
Authors: Forsberg G. , Bednar I. , Qureshi G. A. , Eneroth P. , Sodersten P. 
Published: September 2006

AbstractMethionine‐ and leucine‐enkephalin were measured in the cerebrospinal fluid of lactating rats by high‐performance liquid chromatography and electrochemical detection. The concentration of both peptides was high while the rats were nursing their litter. The concentration of methionine‐enkephalin decreased rapidly when the mother left her litter and increased equally rapidly after mother‐young reunion, provided the pups were allowed direct contact with the nipples of the mother. The level of leucine‐enkephalin did not change during the period of time the lactating rat normally stayed away from its litter but decreased after prolonged (12 h) mother‐pup separation. These results show that the concentration of methionine‐, but not leucine‐enkephalin in the cerebrospinal fluid fluctuates as the lactating rat interacts with its litter and is directly dependent upon the suckling stimulus. Although methionine‐enkephalin may contribute to the inhibition of sexual behaviour which occurs during lactation, the role of the enkephalins in the other behavioural and endocrine adaptations of lactation is unknown.
Oxytocin Receptor Binding in Female Prairie Voles: Endogenous and Exogenous Oestradiol Stimulation
Authors: Witt D. M. , Carter C. S. , Lnsel T. R. 
Published: September 2006

AbstractPrevious studies have demonstrated that oxytocin receptors in specific nuclei of rat forebrain are regulated by gonadal steroids. The current study used in vitro receptor autoradiography to investigate the distribution and regulation of oxytocin receptors in the forebrain of the female prairie vole (Microtus ochrogaster). In contrast to rats, in female prairie voles gonadal steroid secretion and oestrus behaviour result from male chemosignal stimulation and ovulation is induced by mating. Thus, the prairie vole brain provides an opportunity for investigating links between environmental stimuli, gonadal steroids and oxytocin receptors. Using a selective oxytocin receptor ligand [125l]d(CH2)5[Tyr(Me)2,Tyr‐NH29]ornithine vasotocin ([125I]OTA), specific binding was found in several regions including the anterior olfactory nucleus, the ventromedial nucleus of the hypothalamus, the bed nucleus of the stria terminalis, the amygdala and several cortical areas. Following ovariectomy, oestradiol benzoate (10 μg) administration increased oxytocin receptor binding 100% in the anterior olfactory nucleus, but did not affect receptors in other regions. Gonadallyintact females, exposed to male chemosignals, had significant increases in both endogenous oestradiol levels and anterior olfactory nucleus oxytocin receptor binding relative to gonadally‐intact females unexposed to male chemosignals. Following prolonged exposure to males with ad libitum mating, [125I]OTA receptor binding decreased to the levels found in unstimulated females. These results demonstrate that increases in oestrogen levels, of either exogenous or endogenous origin, can modulate oxytocin receptors in the brains of female prairie voles. In contrast to rats, oestrogen in female prairie voles appears to affect receptors in the anterior olfactory nucleus rather than the hypothalamus. We suggest that the species differences in oxytocin receptor distribution and gonadal steroid responsiveness reflect variations in reproductive physiology and possibly behaviour.
Reverse Haemolytic Plaque Assay Study of Corticotropin‐Releasing Hormone and Arginine Vasopressin Interaction in Ovine Corticotropes
Authors: Madsen G. , Chan E‐C. , Falconer J. , Ho K. Y. , Smith R. 
Published: September 2006

AbstractCorticotropin‐releasing hormone and arginine vasopressin are known to interact in stimulating secretion of adrenocorticotropin‐related peptides from corticotropes. However, the mechanism mediating this interaction is uncertain. Recently, evidence has been provided using a reverse haemolytic plaque assay that in rat pituitary cells, arginine vasopressin potentiates the effects of corticotropin‐releasing hormone by increasing the percentage of target cells that secrete adrenocorticotropin. To determine whether a similar mechanism also operates in the sheep corticotrope, which is reportedly more sensitive to arginine vasopressin than that of the rat, a reverse haemolytic plaque assay for β‐endorphin secretion was used to study the response of ovine corticotropes to stimulation by increasing doses of corticotropin‐releasing hormone or arginine vasopressin (0.1 nM to 10.0 nM) alone or in combination.In the reverse haemolytic plaque assay, β‐endorphin antiserum at 1:50 and complement at 1:10 were found to be optimal dilutions for plaque formation. A concentration‐dependent response curve to corticotropin‐releasing hormone was obtained with a significant increase in plaque area from basal to reach maximal levels at 1.0 nM. Arginine vasopressin also stimulated an increase in plaque area, however, plaques formed were significantly smaller than those caused by corticotropin‐releasing hormone. Since in the reverse haemolytic plaque assay, plaque area is related to the amount of hormone secreted by the cell, results demonstrate that although corticotropin‐releasing hormone and arginine vasopressin both stimulate β‐endorphin secretion from ovine corticotropes, corticotropin‐releasing hormone is a more potent secretagogue than arginine vasopressin in that it causes the formation of significantly larger plaques.The addition of arginine vasopressin to low concentrations of corticotropin‐releasing hormone caused plaque areas to reach maximal levels at 0.1 nM whereas these levels were only attained at 1.0 nM when corticotropin‐releasing hormone was used alone. Therefore, arginine vasopressin interacts with corticotropin‐releasing hormone to increase corticotrope responses by increasing their secretory response to corticotropin‐releasing hormone. These data are consistent with previous work suggesting that arginine vasopressin increases the expression of corticotropin‐releasing hormone receptors on the corticotrope cell surface. However, no significant increase in the percentage of plaque‐forming cells was seen with either corticotropin‐releasing hormone or arginine vasopressin alone or in combination implying that there was no recruitment of previously non‐secreting cells.