bluuebunny/crossref_metadata_2025_split huggingface dataset:
Glucocorticoid Effects on the Molecular Forms of Adrenocorticotrophic Hormone Secreted by Cultures of Rat Anterior Pituitary Cell Monolayers
Authors: Norman James C. , Gurney Alison M. , Gillham Brian 
Published: September 2006

AbstractThe effects of glucocorticoids and corticotrophin‐releasing factor (CRF) on the release of various molecular forms of adrenocorticotrophic hormone (ACTH) have been investigated in primary cultures of rat anterior pituitary. The rat cells responded to a 30 min challenge with CRF by secreting increased amounts of ACTH, as assessed both by bioassay, using rat adrenocortical cells, and by radioimmunoassay. Inclusion of a synthetic glucocorticoid, such as dexamethasone (DEX), in the incubation for 5 min prior to, and during the CRF challenge, had no effect on the response as measured by radioimmunoassay. Bioassay, however, indicated profound suppression of the response to CRF. This discrepancy between ACTH immuno‐ and bioactivity was investigated by fractionating the immunoreactive ACTH species using high‐performance liquid chromatography. The lower molecular weight (<15kd) forms (ACTH1–39, phosphorylated ACTH1–39 and glycosylated ACTH1±39) were separated from higher molecular weight (>15kd) forms (i.e. ACTH biosynthetic intermediate and proopiomelanocortin) using C‐18 Sep‐Pak. The lower molecular weight molecules were further resolved into glycosylated and non‐glycosylated ACTH, using an acetonitrile gradient high‐performance liquid chromatography with trifluoroacetic acid as an ion‐pairer. Neither the proportion of low molecular weight forms of ACTH, nor that of glycosylated ACTH1–39 secreted in response to CRF, were affected by DEX. Further fractionation of non‐glycosylated ACTH, also using acetonitrile gradient high‐performance liquid chromatography but with heptafluorobutyric acid as the ion‐pairer, yielded peaks corresponding to phosphorylated and non‐phosphorylated ACTH1–39. DEX significantly increased the proportion of phosphorylated ACTH secreted in response to CRF by 18%. An additional effect of DEX was revealed when Sep‐Pak extracts were treated with alkaline phosphatase, prior to analysis. After dephosphorylation, it became clear that the peptides released by CRF‐stimulated cells were different if DEX was present in the medium. The peptide released in the presence of DEX (ACTH‐S) had a slightly, but consistently, different retention time on high‐performance liquid chromatography and very little biological activity. Antibody cross‐reactivity studies suggested that ACTH‐S was modified in the 1–24 region of the peptide. It is concluded that challenge of anterior pituitary cells in primary culture with CRF, following 5 min previous exposure to DEX, results in a molecular change. The consequence of this is that ACTH immunoreactivity is released, but the molecule has reduced biological activity. This may be part of the mechanism by which fast feedback inhibition of ACTH secretion is effected.
Hemorrhage‐Induced Activations of Adrenocorticotropin Release and Catecholamine Metabolism in the Ventrolateral Medulla are Differently Affected by Glucocorticoid Feedback
Authors: Ponec J. , Lachuer J. , Suaud‐Chagny M. F. , Tappaz M. 
Published: September 2006

AbstractWe have compared the effects of increasing doses of dexamethasone on the hemorrhage‐induced stimulation of the corticotropic axis and the metabolism of the catecholamines of the A1 group in the ventrolateral medulla. Adrenocorticotropin was measured in sequential samples of plasma while the metabolism of the catecholamines was recorded by in vivo electrochemistry in urethane‐anesthetized rats. Combined intracerebroventricular injection of specific adrenergic blockers (α1‐antagonist, prazosin and ß‐antagonist, propranolol) prevented the stimulation of the adrenocorticotropin release by hemorrhage. Pretreatment with dexamethasone (1 mg/kg sc) fully blocked the hemorrhage‐induced adrenocorticotropin release but did not affect the concomitant stimulation of the catecholamine metabolism in A1 cells. The latter was partially decreased only with the highest dose (10 mg/kg sc). While a central catecholaminergic input appears to be necessary for the hemorrhage‐induced stimulation of the corticotropic axis, it does not seem to play a significant role in the feedback regulation by glucocorticoids.
Central Somatostatin Inhibits Cholecystokinin‐lnduced Oxytocin Secretion in Conscious Rats
Authors: Blackburn Ruth E. , Frederick Stephen E. , Strieker Edward M. , Verbalis Joseph G. 
Published: September 2006

AbstractRecent studies have demonstrated the presence of fibres immunoreactive for somatostatin‐28 (SS‐28), which originate in the brainstem and selectively innervate the magnocellular oxytocin (OT) cells of the supraoptic nucleus. The potential physiological relevance of this pathway was investigated in the present study by measuring plasma OT levels in response to intraperitoneal administration of cholecystokinin in conscious male rats pretreated with intracerebroventricular injections of either SS‐28 or artificial cerebrospinal fluid. Cholecystokinin treatment produced the expected marked rise in plasma OT levels in control rats pretreated intracerebroventricularly with artificial cerebrospinal fluid. However, this response was markedly blunted by prior intracerebroventricular administration of SS‐28, even though SS‐28 itself had no effect on basal plasma OT levels, nor did it impair OT release in response to hypertonic saline injection. These results demonstrate that centrally injected SS‐28 can selectively block cholecystokinin‐stimulated release of OT in rats, and support an inhibitory role for this peptide in brainstem‐mediated neurohypophysial hormone secretion.Central SS‐28 administration also elicited up to 3‐fold increases in the amount of food ingested in 1 h by previously sated rats. These observations suggest the possibility that endogenous SS‐28 may be involved in stimulating food intake in rats, and establish the basis for future studies to clarify the role of this neuropeptide in controlling ingestive behaviours.
Effect of Constant Light, Pinealectomy and Guanosine Triphosphate Gamma‐S on the Density of Melatonin Receptors in the Rat Suprachiasmatic Nucleus: A Possible Implication of Melatonin Action
Authors: Gauer F. , Masson‐Pévet M. , Pévet P. 
Published: September 2006

AbstractWe report here the effects of pinealectomy and exposition to constant light on the density of melatonin receptors in the suprachiasmatic nuclei of the rat using quantitative autoradiography. The Bmaxvalues were significantly increased when the animals were maintained in constant light for 3 days (8.22 ± 0.95 fmol/mg protein versus 4.55±0.14 fmol/mg protein in control group, 12 h light/12 h dark cycle (12L/12D), n = 6). A similar increase was also observed in rats pinealectomized 3 days before sacrifice and then maintained either under 12L/12D (Bmax7.56±0.80 fmol/mg protein) or in constant light (Bmax7.85±1.02 fmol/mg protein), while Kdvalues failed to show any variations after constant light and/or pinealectomy.The effect of GTPγS on the density of rnelatonin binding sites was also investigated in control animals and after 3 days of constant light. In 12L/12D animals, the Bmax shifted from 5.94 ± 0.14 fmol/mg protein in the absence of GTPγS to 3.97±0.22 fmol/ mg protein in the presence of 50μiM GTPγS. In animals maintained for 3 days in constant light, a similar decrease in the Bmax value was observed (8.95 ± 0.25 fmol/mg protein in absence and 5.95 ± 0.22 fmol/mg protein in presence of 50 μ GTPγS). In both cases, Kd values were not affected by GTPγS.Pinealectomy and constant light exposition are known to induce a suppression of the nocturnal peak of plasma rnelatonin and to keep plasma rnelatonin concentrations at a very low level. These results could suggest a regulatory effect of rnelatonin on the density of its own receptors which are shown here to be also coupled with a G‐protein.
Characterization of the Parabrachial Nucleus Input to the Hypothalamic Paraventricular Nucleus in the Rat
Authors: Jhamandas Jack H. , Harris Kim H. , Petrov Theodor , Krukoff Teresa L. 
Published: September 2006

AbstractThe brainstem parabrachial nucleus (PBN) is viewed as an increasingly important site for the transfer of autonomic‐related information to more rostral structures in the forebrain including the hypothalamus. In this study, we examined electrophysiologically in vivo and anatomically the nature of PBN input to the hypothalamic paraventricular nucleus (PVN) and particularly to the vasopressin‐and oxytocin‐secreting magnocellular neurosecretory cells within this nucleus.In urethane‐anaesthetized rats, extracellular recordings from 108 antidromically identified neurosecretory PVN cells revealed an excitatory (37/43 cells) and less frequently an inhibitory (6/43 cells) response consequent to electrical stimulation in the PBN. Both vasopressin (12/37 cells)‐and oxytocin (9/37 cells)‐secreting neurons appear to respond to the PBN stimulus. Four cells projecting to the neurohypophysis could also be antidromically activated from PBN, and this observation may be indicative of collateral branching in some PVN neurosecretory neurons. In addition, recordings from 60 non‐magnocellular (i.e. non‐neurohypophysially‐projecting) PVN cells revealed a facilitatory response (43/60 cells) following PBN stimulation, Iontophoretic injections of the anterograde tracer Phaseolus vulgaris leucoagglutinin (PHA‐L) were made within the rat lateral PBN and brains prepared for immunocytochemical examination of projections to the PVN region. PHA‐L‐labelled fibres and terminals were visualized within both the parvocellular and magnocellular divisions of the PVN. In addition, labelled fibres were also seen in a region immediately dorsal to the PVN. PHA‐L‐labelled fibres with axonal varicosities and boutons were visualized over immunocyto‐chemically‐identified vasopressin and oxytocin neurons within the magnocellular PVN. These convergent electrophysiological and anatomical data provide evidence for a PBN projection to the PVN that is predominantly excitatory to both magnocellular neurosecretory and non‐magnocellular cells. Moreover, with respect to vasopressin‐and oxytocin‐secreting cells, the PBN input appears to be directed at both populations of peptidergic neurons.
Electrical Activity of Dorsal Horn Neurons During the Suckling‐Induced Milk Ejection Reflex in the Lactating Rat
Authors: Fénelon Valérie S. , Poulain Dominique A. 
Published: September 2006

AbstractIn lactating rats, suckling elicits the milk ejection reflex which consists of an intermittent synchronous activation of hypothalamic oxytocin neurons which releases oxytocin into the bloodstream. We here investigated the electrophysiological behaviour of spinal cord neurons linked to mammary innervation in relation to suckling and the suckling‐induced milk ejection reflex. Experiments were carried out on 58 urethane‐anaesthetized rats, paralysed with gallamine triethiodide and artificially ventilated. Fixation of the spinal cord and laminectomy significantly slowed down the reflex, which occurred in only 27% of the animals. In these rats, 31 dorsal horn neurons at the thoraco‐lumbar level were found to be excited by nipple stimulation. During suckling by a litter of at least nine pups, they displayed an irregular pattern of brief bursts of activity (peak firing rate 22.0 ± 3.2 Hz, mean ± SD) correlated to the bouts of suckling of the pups. Seventeen out of 19 cells tested by stimulation of at least 2 adjacent nipples received convergent input from different ipsilateral nipples. Out of 11 cells tested, 8 were also activated by stimulation of a contralateral nipple. Fourteen out of 30 units were recorded through at least one reflex milk ejection. Their firing rate was significantly higher than the firing rate of cells recorded in animals which failed to milk eject (4.4 Hz ± 2.8 versus 1.5 Hz ± 0.7). At the moment of the high frequency discharge of action potentials, occurring in oxytocinergic cells 10 to 15 s before each milk ejection, spinal neurons showed no systematic change in electrical activity. In contrast, the stretch reaction of the pups, which corresponds to an intense period of suckling when milk ejection has started, induced, in 12 cells, a considerable increase in electrical activity. One unit was found to be inhibited by suckling and during the stretch reaction. Ten more units, which were not activated by stimulation of the nipples but responded to stimulation of excitatory receptive fields near the last three pairs of nipples, were recorded through reflex milk ejections: 8 remained silent during reflex milk ejections but 2 were activated when the pups stimulated their excitatory receptive field. We conclude that some dorsal horn neurons, able to respond readily to the suckling movements of pups, appear to receive an ungated input from the nipples. At the time of the activation of oxytocin neurons, they present no particular pattern of activation or inhibition which could account in a simple manner for the intermittence of the high frequency discharge in oxytocinergic cells. However, in so far as these dorsal horn neurons may be part of the milk ejection reflex pathway, their activity, showing convergence and summation of input, and being facilitated in milk ejecting animals, indicates that the reflex does undergo a certain degree of processing at the spinal cord level.
C‐Type Natriuretic Peptide Stimulates Prolactin Secretion by a Hypothalamic Site of Action
Authors: Huang Fong‐Lee S. , Skala Karl D. , Samson Willis K. 
Published: September 2006

AbstractThe most recently discovered member of the family of natriuretic peptides, C‐type natriuretic peptide (CNP), exerts many pharmacologic actions similar to its structural homolog A‐type natriuretic peptide (ANP). Like ANP it failed to significantly alter prolactin release from dispersed, rat anterior pituitary cells incubated under static or dynamic conditions. Unlike ANP, however, which inhibits prolactin secretion in vivo by a hypothalamic action, CNP injection into the third cerebroventricle significantly stimulated prolactin secretion in ovariectomized, conscious rats. The effect was highly significant 15 min after injection and transient, lasting 30 min in animals injected with 2 nmole CNP. In a companion group of rats, significant inhibition of plasma prolactin levels was observed after central administration of similar doses of ANP. These results suggest differing hypothalamic actions of the CNP and ANP perhaps mediated by multiple natriuretic peptide receptors present in the tissue. Further, they provide additional support for unique roles exerted within the central nervous system by these structural homologs.
Central Administration of Serotonin Decreases Tyrosine Hydroxylase Catalytic Activity and Messenger Ribonucleic Acid Signal Levels in the Hypothalamus of Female Rats
Authors: Mathiasen Joanne R. , Arbogast Lydia A. , Voogt James L. 
Published: September 2006

AbstractWe investigated the effect of central serotonin (5‐hydroxytryptamine, 5‐HT) administration on hypothalamic tuberoinfundibular dopamine neurons and related changes in neuronal activity to circulating prolactin (PRL) levels. Ovariectomized rats were treated with either vehicle or 5‐HT through a lateral ventricular cannula in one of two dose paradigms: 1) a bolus of 20 μg, with tissues taken at 30 min, or 2) the same bolus immediately followed by 20 μg/30 min via a syringe pump for 120 min, and tissues taken at 120 min. Blood samples were taken throughout experiments and plasma PRL determined by radioimmunoassay. Under both paradigms, NSD 1015, a dihydroxyphenylalanine (DOPA) decarboxylase inhibitor (25 mg/kg intraarterially) was injected 10 min before decapitation and brain excision followed by stalk‐median eminence dissection. The rate of DOPA accumulation, determined by measuring DOPA levels in the stalk‐median eminence by high‐performance liquid chromatography with electrochemical detection was used as a measure of tyrosine hydroxylase (TH) catalytic activity. Stalk‐median eminence DOPA accumulation in control rats was 29.9 ± 4.2 and 28.8 ± 4,4 ng/mg protein (30 and 120 min experiments, respectively). DOPA accumulation in 5‐HT‐treated rats was significantly reduced (P<0.05) after 30 min to 17.8 ± 1.2 ng/mg protein, but it was similar (21.7 ± 3.9) to controls after 120 min of 5‐HT infusion. 5‐HT levels in the stalk‐median eminence of rats treated with 5‐HT were 13‐ to 17‐fold greater than controls (16.9 to 18.5 ng/mg protein). Plasma PRL levels in both groups increased 10‐fold after 5‐HT treatment with a peak at 5 min, returning to baseline by 120 min. TH mRNA levels were determined by in situ hybridization in a second group of rats which were treated with the 20μg bolus and subsequent 120 min infusion of 5‐HT. TH mRNA signal levels in the arcuate nucleus of control rats averaged 144 ± 21 grains/cell. After treatment with 5‐HT, TH mRNA levels in the arcuate nucleus were significantly lower (P<0.0001) with 69±14 grains/cell. In a third group of rats, the effects of the 30 min 5‐HT treatment on TH catalytic activity and circulating PRL levels was challenged with two 5‐HT2 receptor antagonists, LY53857 (5 mg/kg intraperitoneally) or ketanserin (10 mg/kg intraperitoneally). Neither the 5‐HT‐induced decrease in TH catalytic activity nor the increase in PRL was altered by pretreatment (120 min) with 5‐HT2 antagonists. These data suggest that central 5‐HT is capable of decreasing TH activity and TH mRNA levels in the tuberoinfundibular dopamine neurons and that the decrease in dopaminergic neuronal activity may contribute to the 5‐HT‐induced PRL rise. The changes in TH catalytic activity and PRL after intracerebroventricular administration of 5‐HT do not appear to be mediated by 5‐HT2 receptors.
Neuropeptide Y‐lmmunoreactive Nerve Fibres in the Pineal Gland of the Macaque (Macaca fascicularis)
Authors: Mikkelsen Jens D. , Mick Gérard 
Published: September 2006

AbstractThe distribution of neuropeptide Y (NPY)‐ and the C‐fianking peptide of NPY (CPON)‐immunoreactive elements in the pineal gland of the macaque was investigated by means of immunohistochemistry. NPY‐ and CPON‐immunoreactive nerve fibres were located in the precommissural nucleus, around the stria medullaris, and in the posterior commissure. NPY‐ and CPON‐immunoreactive nerve fibres endowed with bulbous varicosities, were traced from the brain via the pineal stalk into the rostral part of the pineal gland. Furthermore, CPON‐immunoreactive, and to a lesser extent NPY‐immunoreactive nerve fibres, were distributed in the méninges, the choroid plexus and the vasculature related to the pineal organ. Nerve fibres located in the pineal capsule penetrated into the pineal parenchyma, where groups of individual fibres were found most often in an interlobular position. Occasionally, individual nerve fibres dispersed between the pinealocytes were observed. In contrast to the nerve fibres originating from the brain, those originating from the periphery were endowed with smaller immunoreactive nerve terminals. Another apparent difference was that the peripheral nerve fibres innervated only the caudal two‐thirds of the gland, whereas the central fibres were found exclusively in the rostral part of the pineal organ. Rarely, positive neuronal‐like cells were found in the pineal parenchyma. These results show the presence of a moderate number of NPY‐ and CPON‐immunoreactive nerve fibres within the primate pineal organ and strongly indicate that the primate pineal gland is innervated by NPYergic nerve fibres originating from both a peripheral and a central source.
Effects of Ibotenic Acid‐Induced Neuronal Degeneration in the Hypothalamus upon Proceptivity and Sexual Receptivity in the Female Marmoset (Callithrix jacchus)
Authors: Dixson A. F. , Hastings M. H. 
Published: September 2006

AbstractThe sexual behaviour of 16, oestradiol‐treated, ovariectomized common marmosets was recorded before and after bilateral microinfusions of ibotenic acid (n = 8) or isotonic saline (n = 8) into the hypothalamus. Ibotenic acid‐induced neuronal degeneration occurred in 5 females, mainly affecting the anterior and dorsomedial hypothalamus. Marked decreases in proceptivity (tongue‐flicking, staring and immobile displays) occurred after ibotenic acid lesions, whereas sexual receptivity (refusals and terminations of male partners' mounts) was unchanged. In 3 females where microinfusions of ibotenic acid were attempted but failed to produce lesions, sexual behaviour was unaffected and resembled that measured in saline‐treated controls. These results provide the first evidence that selective lesions of neuronal cell bodies in the anteromedial hypothalamus disrupt proceptivity whilst sparing sexual receptivity in a primate species.
Luteinizing Hormone‐Releasing Hormone Neurons which are R‐etrogradely Labeled After Peripheral Fluoro‐Gold Administration in the Male Ferret
Authors: Berglund Lee Ann , Sisk Cheryl L. 
Published: September 2006

AbstractThis study identified luteinizing hormone‐releasing hormone (LHRH)‐producing neurons which have access to fenestrated capillaries in prepubertal male European ferrets. Fluoro‐Gold was injected intraperitoneally to retrogradely label neurons with terminals outside the blood‐brain barrier. LHRH neurons were identified by immunofluorescence using a secondary antibody tagged with tetramethylrhodamine isothiocyanate. Cell bodies which demonstrated both tetramethylrhodamine isothiocyanate and Fluoro‐Gold fluorescence were defined as LHRH‐producing neurons with axon terminals in regions containing fenestrated capillaries. The total number and neuroanatomical distribution of immunopositive (LHRH +) cells concurred with previous studies in the ferret in which cell bodies were diffusely distributed from rostral forebrain through caudal diencephalon, with approximately 70% of the LHRH + cell bodies located in retrochiasmatic hypothalamus. In the present study, an average of 59.8% of all LHRH+ neuronal perikarya also contained Fluoro‐Gold. The majority of Fluoro‐Gold filled LHRH+ neurons demonstrated only faint to moderate amounts of Fluoro‐Gold when compared to other Fluoro‐Gold filled neurosecretory neurons. This limited uptake of Fluoro‐Gold may be due to a relative inactivity of LHRH neurons projecting outside the blood‐brain barrier. Double‐labeled LHRH + neurons were dispersed throughout the entire population of LHRH+ cell bodies and no apparent nuclear groups of double‐labeled neurons were found. This observation suggests that the LHRH+ neurons responsible for neurosecretion into the median eminence coexist with the LHRH+ neurons responsible for intracerebral neurotransmission or neuromodulation. One distinguishable population of LHRH + neurons was consistently observed in all the brains. Only 26% of total LHRH+ perikarya within the caudal arcuate nucleus contained Fluoro‐Gold, while at least 50% of LHRH+ neurons in other structures, including the rostral arcuate nucleus, contained Fluoro‐Gold. Thus, in the prepubertal male ferret, the majority of LHRH cell bodies located in the caudal arcuate nucleus may be differentially regulated and/or involved in non‐neuroendocrine functions.