bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stress‐Induced Oxytocin Release in the Rat After Lesion of the Paraventricular Nuclei; Possible Deficiency of Corticotrophin‐Releasing Factor
Authors: Higuchi Takashi , Honda Kazumasa , Takano Shin , Negoro Hideo 
Published: September 2006

AbstractOxytocin is released under stressful conditions and corticotrophin‐releasing factor (CRF) is known to be involved in mediating general ‘stress responses’. We therefore examined whether CRF neurons in the paraventricular nucleus participate in the stress‐induced oxytocin release in the rat. CRF (0.02 to 2 nmol) injected into the third ventricle produced a dose‐dependent rise in the plasma oxytocin concentration. The oxytocin release induced by CRF occurred without a change in blood pressure, and was not affected by dexamethasone pretreatment, which prevents adrenocorticotrophin release following CRF injection. Lesioning of the paraventricular nucleus reduced oxytocin release by immobilization stress, but did not alter the release of oxytocin in response to osmotic stimulation induced by intraperitoneal injection of hypertonic saline. Anti‐CRF serum injection into the third ventricle reduced delayed oxytocin response to immobilization stress. These results are consistent with the hypothesis that CRF neurons in the paraventricular nucleus are involved in the oxytocin release during immobilization stress in the rat.
Vasotocin Target Sites in the Capsular Region Surrounding the Nucleus Robustus Archistriatalis of the Canary Brain
Authors: Voorhuis T. A. M. , Elands J. P. M. , De Kloet E. R. 
Published: September 2006

AbstractThe aim of this study was to characterize neurohypophyseal hormone receptors in the brain of the canary (Serinus canarius) by using autoradiographical and biochemical procedures with a radioiodinated vasotocin analogue, [125 l]d(CH2)5[Tyr(Me)2, Thr4, Orn8, Tyr‐NH29]vasotocin ([125 I]‐OTA). This synthetic analogue was used previously to identify a population of oxytocin‐like receptors in the rat brain that have high affinity for vasotocin. In vitro autoradiography revealed high affinity binding sites for [125 I]‐OTA in the canary brain in the archistriatum surrounding the nucleus robustus archistriatalis. Scatchard analysis of [125 I]‐OTA binding to a synaptic membrane fraction prepared from the archistriatal region including the nucleus robustus archistriatalis indicated the presence of a single population of binding sites (Kd= 0.05 nM; Bmax= 4 fmol/mg protein).Displacement studies revealed that the order of potency of certain peptides to inhibit [125 I]‐OTA binding was as follows: vasotocin (Ki= 0.4 nM) > oxytocin = vasopressin > mesotocin (Ki= 8.0 nM). The administration of testosterone to female canaries did not affect [125 I]‐OTA labelling in the archistriatum detected by autoradiography and did not influence [125 I]‐OTA binding constants in the membrane binding assay. In conclusion, this study provides morphological and biochemical evidence of a vasotocin‐target site in the archistriatum in close association with the central vocal control circuit in the canary brain.
Non‐Phasic Discharge and Osmoresponsiveness of Cat Magnocellular Neuroendocrine Cells
Authors: Fagan M. , Andrew R. D. 
Published: September 2006

AbstractRepetitive bursting (phasic firing) generated endogenously by magnocellular neuroendocrine cells (MNCs) in the rat facilitates systemic release of vasopressin from axon terminals in the neurophypophysis. However, little is known of how MNCs function in other mammals. Using coronal slices of hypothalamus we studied the firing behaviour and intrinsic membrane properties of homologous neurons in the cat supraoptic nucleus where vasopressinergic MNCs outnumber oxytocinergic cells. Less than 1% of units recorded in cat supraoptic nuclei (2 of 270) spontaneously fired in a phasic mode compared to 39% in the rat (90 of 230). A discrete level of steady current across the extracellular recording micropipette promoted phasic firing in 66 of 152 non‐phasic units tested in rat supraoptic nuclei, but no phasic activity in 189 units from the cat. One or several stimuli applied dorsal to supraoptic nuclei triggered a single burst (afterdischarge) in 115 of 180 MNC units from the rat, whereas none of 173 MNC units tested in the cat fired an afterdischarge. Intracellular recordings from 56 feline MNCs revealed that unlike the rat, spike depolarizing afterpotentials were absent in all cells. This explains both the absence of phasic firing and the inability to trigger regenerative bursts in the intact cat. The possible Osmoresponsiveness of cat MNCs was examined using unit recording. These units reversibly increased their firing rate as osmolality was elevated with mannitol or NaCl (10 to 100 mOsm/kg), comparable to rat units. However, in no case did hyperosmotic conditions elicit phasic firing. We conclude that cat MNCs lack a regenerative burst capability but that unit Osmoresponsiveness is comparable to rat MNC units. We hypothesize that since the kidney of the cat normally functions at high efficiency in terms of water resorption, there may be little need for the rapid and pronounced elevation in vasopressin release evoked by phasic firing.
Control of Phospholipid Turnover and Prolactin Release in a Dopamine‐Sensitive, Prolactin‐Secreting Rat Pituitary Adenoma and in Two Dopamine‐Resistant, Prolactin‐Secreting Rat Pituitary Tumors
Authors: Forget H. , Huot C. , Collu R. 
Published: September 2006

AbstractThe secretion of prolactin by the pituitary gland is under a tonic inhibitory control exerted by tubero‐infundibular dopamine. Recently, it has been suggested that dopamine may exert its action by inhibiting production of inositol phosphates and mobilization of intracellular Ca2+. To study the effects of dopamine on the production of inositol phosphates and prolactin release, we have utilized an estrone‐induced, dopamine‐sensitive rat pituitary adenoma and two transplantable and dopamine‐resistant rat pituitary tumors, 7315a and MtTW15. Purified cells, obtained from the three tissues, were incubated for 30 min in media with drugs (thyrotropin‐releasing hormone or angiotensin II) stimulating inositol phosphates and prolactin release, in the presence or the absence of dopamine. Basal production of inositol phosphates and prolactin release by adenomatous lactotrophs were inhibited by dopamine. Thyrotropin‐releasing hormone and angiotensin II stimulated inositol phosphates by adenomatous and 7315a cells. This effect was antagonized by dopamine in adenomatous cells. Prolactin release by adenomatous cells only was stimulated by thyrotropin‐releasing hormone and angiotensin II. This stimulation was inhibited by dopamine. The results show differences, in the mechanisms of regulation of prolactin release, between adenoma and transplantable pituitary tumors as well as between the two tumors themselves. These differences may be responsible, in part, for the resistance of the two transplantable pituitary tumors to the inhibitory effects of dopamine on prolactin release and tumor size. Our results obtained both with adenoma and tumoral cells also suggest that inositol phosphates probably intervene only in the late phases of dopamine inhibition of prolactin release and only in the presence of a normal Ca2+ signaling system.
Vasopressin Expression in Cultured Neurons is Stimulated by Cyclic AMP
Authors: Ceding Petra , Schilling Karl , Schmale Hartwig 
Published: September 2006

AbstractVasopressin and oxytocin genes are expressed in mutually exclusive sets of magnocellular neurons in the hypothalamus. Cell specificity and regulation are probably controlled by extra‐ and intracellular signals acting on one or the other gene. In order to identify factors that regulate peptide expression, we have used primary dissociated cultures derived from 14‐day old foetal rats. Vasopressin expression was monitored by combined immunocytochemistry and in situ hybridization. Treatment of cultures with forskolin and/or the phosphodiesterase inhibitor 3‐isobutyl‐1‐methylxanthine (IBMX), both of which result in elevated intracellular cyclic AMP levels, increased the numbers of vasopressin‐expressing cells up to 10‐fold. The specific Vasopressin messenger ribonucleic acid accumulation was verified quantitatively by ribonuclease protection assays. Forskolin and IBMX did not change the levels of the general neuronal markers, neuron‐specific enolase and synaptophysin, suggesting that the effect of these drugs was specific for vasopressin‐expressing cells. The drugs were not mitogenic for magnocellular neurons. Furthermore, their effect was not mediated trans‐synaptically, as the drugs were also effective in cultures grown in low Ca2+/high Mg2+ medium, as well as in cultures treated with either tetanus toxin or tetrodotoxin. The presence of putative response elements for the transcription factor AP‐2 in the 5’promoter regions of all vasopressin genes sequenced so far may provide the molecular basis of the observed cyclic AMP effect. No such elements are present in the genes for oxytocin, the messenger ribonucleic acid levels of which were not measurably affected by forskolin and IBMX in our cultures.
Central 5,7‐Dihydroxytryptamine Lesions Decrease Hippocampal Glucocorticoid and Mineralocorticoid Receptor Messenger Ribonucleic Acid Expression
Authors: Seckl Jonathan R. , Dickson Karen L. , Fink George 
Published: September 2006

AbstractCorticosteroids exert effects on the hippocampus by binding to intracellular glucocorticoid and/or mineralocorticoid receptors, but the relative importance of each receptor type in mediating corticosteroid effects is poorly understood. There is an extensive serotoninergic (5‐HT) innervation of the hippocampus which interacts with corticosteroid‐sensitive cells. We have investigated the effect of intracerebroventricular 5,7‐dihydroxytryptamine lesions of 5‐HT neurons on glucocorticoid and mineralocorticoid receptor messenger ribonucleic acid (mRNA) expression in the rat hippocampus using in situ hybridization histochemistry. In controls, glucocorticoid receptor mRNA was highly expressed in dentate gyrus granule cell neurons, and in pyramidal cells of CA1 and CA2, but levels in CAS and CA4 were significantly lower. 5,7‐dihydroxytryptamine‐lesioned animals showed significantly less glucocorticoid receptor mRNA in the dentate gyrus (76% decrease), CA1 (42% decrease) and CA2 (52% decrease; all P<0.05 compared with controls). Mineralocorticoid receptor mRNA was expressed at a similar level in all hippocampal subregions in control rats. 5,7‐dihydroxytryptamine lesioning led to a significant decrease in mineralocorticoid receptor mRNA expression in CA3 (56% fall) and CA4 (45% fall; both P<0.05), but not in the other subregions. Thus the 5‐HT innervation regulates hippocampal corticosteroid receptor mRNA expression.
Vaginocervical Stimulation of Ferrets Induces Release of Luteinizing Hormone‐Releasing Hormone
Authors: Bibeau Carole E. , Tobet Stuart A. , Anthony Edythe L. P. , Carroll Rona S. , Baum Michael J. , King Joan C. 
Published: September 2006

AbstractVaginocervical stimulation of ovariectomized estradiol‐primed ferrets (which are reflex ovulators) with a glass rod in the presence of a neck‐gripping male induced an increase in plasma luteinizing hormone (LH) from undetectable levels (≤0.50 ng/ml) before stimulation, to 2.4 ± 0.43 ng/ml 75 min after stimulation (stimulated females). Forty‐eight h after stimulation plasma LH returned to baseline levels (post‐stimulated females). A significant decrease in the number of perikarya containing LH‐releasing hormone (LHRH), detected by immunocytochemistry, was associated with the increase in plasma LH following stimulation. Approximately one half of the number of immunoreactive LHRH neurons (243±27) were detected in the forebrain of stimulated females, compared to those detected in the forebrain of post‐stimulated animals (436 ± 88) using antiserum AR 744. Equivalent results were obtained with a different antiserum (RM 1076) capable of detecting the extended decapeptide, or precursor, as well as partially or fully processed decapeptide.We conclude that controlled Vaginocervical stimulation of female ferrets evokes the release of LHRH as well as LH, depleting approximately 50% of the LHRH perikarya of detectable LHRH. Additionally, electron microscopy of LHRH perikarya of stimulated females revealed more Golgi complexes/cell compared to baseline females. We propose that Vaginocervical stimulation also augments the processing of extended precursor forms of LHRH to generate the decapeptide.
Diurnal Differences and Adrenal Involvement in Calmodulin Stimulation of Hippocampal Adenylate Cyclase Activity
Authors: Gannon Maureen N. , Brinton Roberta E. , Sakai Randall R. , McEwen Bruce S. 
Published: September 2006

AbstractCalciam/calmodulin‐dependent processes are altered by manipulations of the hypothalamic‐pituitary‐adrenal axis, and are associated with changes in synaptic efficacy in the hippocampus, such as long‐term potentiation. Recent evidence indicates that there are diurnal variations in the threshold for long‐term potentiation, as well as diverse effects of the adrenals and of adrenal steroids on electrical activity related to long‐term potentiation. In order to probe possible mechanisms underlying these observations, we investigated the effects of the diurnal cycle, as well as adrenalectomy (ADX) and adrenal demedullation on adenylate cyclase activity. In hippocampal, but not cortical, membranes the adenylate cyclase response to calmodulin was higher during the beginning of the dark phase of the cycle, when endogenous corticosterone levels are high. Basal and forskolin‐stimulated adenylate cyclase activity did not exhibit diurnal variation in either brain region. ADX (6 and 14 days) depressed the adenylate cyclase response to calmodulin in hippocampal membranes, and abolished the diurnal difference. ADX had smaller effects on this response in cortical membranes. ADX also attenuated basal and forskolin‐stimulated adenylate cyclase activity, but these changes were less striking than effects on calmodulin‐stimulated activity. Demedullation (14 days), generating corticosterone levels in the low physiological range, mirrored the effects of ADX on hippocampal adenylate cyclase activity. Corticosterone (20 to 25 μg/ml in the drinking water) did not consistently prevent ADX effects on adenylate cyclase activity. These results demonstrate that adrenal effects on adenylate case activity are regionally specific within the brain, and they suggest that other adrenal secretions besides glucocorticoids may be involved in the feedback of the diurnal rhythm on the hippocampus. Taken together with our recent finding that chronic stress or corticosterone injection selectively attenuated the adenylate cyclase response to calmodulin in cortical, but not hippocampal membranes our findings provide further support for a role of the pituitary‐adrenal axis in modulating neural calmodulin‐dependent adenylate cyclase activity.
Enhanced Neurohypophyseal Vasopressin Release is Associated with Increased Opioid Inhibition of Oxytocin Release
Authors: van de Heijning Bert J. M. , den Herik Ineke Koekkoek‐van , Rots Nynke Y. , Greidanus Tjeerd B. van Wimersma 
Published: September 2006

AbstractWe tested the hypothesis of a cross‐inhibition of oxytocin (OT) release by endogenous opioid peptides co‐released with vasopressin (VP). This opioid cross‐inhibition resulted in a selective block of OT release and hence in preferential release of VP.The effects of the opiate receptor antagonist naloxone were tested on neurohypophyseal VP release during dehydration, ethanol administration and sulphated cholecystokinin octapeptide (CCK‐8S) application, assuming that the inhibition of pituitary OT release by endogenous opioids increases as neurohypophyseal VP output increases.A high VP output was found to coincide with increased inhibition of OT release: Subcutaneous injection of graded doses of naloxone (30 min prior to decapitation), augmented OT plasma levels significantly more in 24 h water‐deprived male rats than in normally hydrated rats. Naloxone had no effect on VP release.Ethanol (10% in saline) administered intragastrically 50 min prior to decapitation and 20 min before subcutaneous naloxone (5 mg/kg) resulted in the inhibition of VP output. The ethanol treatment resulted in a rise in plasma OT levels that was additional to the effect of naloxone. These features were present in normally hydrated as well as in 24 h water‐deprived animals, but were more pronounced in the latter group.Peripheral CCK‐8S administration induces an abrupt and selective secretion of OT. Blocking the opioid inhibition of OT release with naloxone resulted in a significant rise of OT compared to that with CCK‐8S alone. The magnitude of the opioid inhibition coincided with the activity of the VP system, and a higher dose of naloxone was needed to potentiate the CCK‐8S effect on OT release in the water‐deprived group than in euhydrated rats. No effect of CCK‐8S and/or naloxone was found on VP plasma levels.The data indicate that opioid peptides co‐released with VP (like dynorphin) may be responsible for cross‐inhibition of OT release during dehydration. This suggests that dynorphin acts in a paracrine way, making it a strong candidate for this role.
Adrenocorticotropin Hyperresponsiveness in Myotonic Dystrophy Following Oral Fenfluramine Administration
Authors: Grice Jeffrey E. , Jackson Jane , Penfold Paula J. , Jackson Richard V. 
Published: September 2006

AbstractThe plasma immunoreactive adrenocorticotropin and cortisol responses to oral fenfluramine hydrochloride (1.5mg/kg body wt) or placebo were examined in 11 patients with myotonic dystrophy, 4 controls with facioscapulohumeral dystrophy, a similarly debilitating muscle wasting disease, and 14 normal controls in single‐blind studies performed in mid‐afternoon.Mean areas under the adrenocorticotropin response versus time curve were significantly greater in myotonics (2573 + 429 pmol.min/L) than in facioscapulohumeral dystrophy controls (696 + 279 pmol.min/L, P<0.02) and normals (560±61 pmol.min/L, P<0.0001). Corresponding cortisol responses were significantly greater in myotonics (35757 + 3949 nmol.min/L) than in normals (21828±1669 nmol.min/L, P < 0.001), but not significantly greater than those in facioscapulohumeral dystrophy controls (22830 + 6140 nmol.min/L, P = 0.055). No stressful side‐effects which could affect hormone responses, and no significant changes in blood pressure or heart rate were noted.Fenfluramine activates central serotonergic and/or noradrenergic pathways initiating secretion of corticotropin‐releasing hormone and possibly arginine vasopressin. We postulate that these fenfluramine‐activated pathways are hyperstimulated in myotonics, leading to adrenocorticotropin and cortisol hypersecretion. This may be a manifestation of a general cell membrane defect in myotonic dystrophy. We found a lack of correlation of age (and severity of disease) with adrenocorticotropin response in myotonics, and therefore, the hyperresponse may serve as a useful marker for the disease before development of other overt signs.
Acute Action of Oestrogen on Medial Preoptic Gamma‐Aminobutyric Acid Neurons: Correlation with Oestrogen Negative Feedback on Luteinizing Hormone Secretion
Authors: Herbison Allan E. , Heavens Robert P. , Dye Sandra , Dyer Richard G. 
Published: September 2006

AbstractThe acute effects of oestrogen on the medial preoptic area (MPOA) γ‐aminobutyric acid (GABA) system were examined by delivering an intravenous bolus of 17β‐oestradiol (5 μg/100 g body wt) to conscious ovariectomized rats implanted with microdialysis probes. Fifteen‐min blood samples were taken to determine the time‐course of negative feedback effects of oestrogen on luteinizing hormone (LH) secretion. Two h after administration of 17β‐oestradiol, GABA release from the MPOA was significantly elevated compared with vehicle‐treated controls (P<0.05). The rise in GABA levels continued until the end of the experiment, 4 h after 17β‐ oestradiol, at which time it was over 50% higher than controls (P<0.01). The pulsatile pattern of LH secretion was significantly depressed 2 and 3 h after administration of 17β‐oestradiol compared with controls (P<0.05). To determine the effects of the 17β‐oestradiol treatment on pituitary responsiveness to LH‐releasing hormone (LHRH), a further group of rats were given exogenous LHRH (50ng/100g body wt, intravenously) before and 3 h after vehicle or 17β‐oestradiol treatment and blood samples taken to determine the effect on LH secretion. The maximal LH response to LHRH in 17β‐oestradiol‐treated rats was approximately 50% that of control‐treated values. This study demonstrates the acute and potent action of 17β‐oestradiol on GABA release in the MPOA and lends support to a genomic site of action for oestrogen in modulating neural elements regulating GABA release from the MPOA. These results, showing a parallel decrease in LH secretion with increased GABA levels in the MPOA, suggest a role for GABA elements within the MPOA as a site of oestrogen negative feedback on LH secretion.
Effect of Chronic Nicotine Treatment and its Withdrawal on the Vasopressinergic System in Rats
Authors: Zbuzek Vlasta K. , Zbuzek Vratislav 
Published: September 2006

AbstractWe have studied the effect of chronic nicotine treatment and its withdrawal on the hypothalamo‐neurohypophyseal Vasopressinergic system in male Sprague‐Dawley rats. They were subcutaneously infused with low and high doses of nicotine, free base (0.6 and 6.0 mg/kg/day, respectively) for 28 days, via Alzet osmotic pumps. The studies were carried out immediately after the period of infusion and 1, 7, 14 and 28 (the latter in high dose only) days later. Basal, high K+‐stimulated and total vasopressin release from the superfused neural lobes, the residual vasopressin content in the neural lobes, and hypothalamus and plasma vasopressin concentration were measured by radioimmunoassay.Treatment with the high dose of chronic nicotine alone decreased vasopressin content in and release from the neural lobe and its plasma concentration, but it did not change significantly the vasopressin content in the hypothalamus. A similar pattern of changes in vasopressin release and plasma concentration, though less pronounced, was observed in the rats infused with the low dose of nicotine.The withdrawal of the high dose of chronic nicotine gradually returned the decreased plasma vasopressin concentration, and its content in and release from the neural lobe to control values within 2 weeks. However, vasopressin content in the hypothalamus started to decline 1 week after nicotine withdrawal and persisted to decline for at least 3 subsequent weeks. The withdrawal of the high dose was associated with a marked suppression of high K+‐stimulated vasopressin release from the neural lobe for a period of 4 weeks. The withdrawal of the low dose of nicotine exhibited a significant decline in plasma vasopressin concentration for up to 2 weeks only following chronic nicotine withdrawal, tending to return subsequently to control levels.