bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lack of Glucocorticoids Enhances the Early Activation of the Medullary Catecholaminergic Cell Groups Triggered by Restraint Stress
Authors: Lachuer Joël , Buda Michel , Tappaz Marcel 
Published: September 2006

AbstractWe have investigated whether the stress‐induced activation of the medullary catecholaminergic neurons, that was shown previously to provide the main central activation input to the hypothalamo‐pituitary‐adrenocortical axis during an immobilization stress, is sensitive to circulating corticosteroids. Experiments were carried out on adrenalectomized rats that were first maintained on corticosterone in the drinking water for 5 days following surgery and then switched to corticosterone‐free water 15 h before stress application. Some of the latter animals were injected with dexamethasone. Activation of the brainstem Catecholaminergic neurons was estimated by assaying 3,4‐dihydroxyphenylacetic acid (DOPAC), a side metabolite of the noradrenaline and adrenaline biosynthesis pathway that was established previously as a reliable index of the activity of these neurons. In the so‐called A1C1 and A2C2 Catecholaminergic groups of the medulla, lack of corticosterone under these experimental conditions did not modify the basal level of DOPAC but led to a further enhancement (+ 35% to 40%) of the approximately 2‐fold increase in DOPAC content observed 15 min after the onset of the 5‐min immobilization stress. No significant further enhancement of the stress‐induced DOPAC increase was observed in the locus coeruleus. In these adrenalectomized rats, dexamethasone pretreatment prevented the enhancement of the stress‐induced increase in DOPAC level observed in the medullary cell groups but did not abolish the response to stress. Lack of endogenous corticosteroids led to a 10‐fold enhancement of the adrenocorticotropin increase following immobilization stress. Pretreatment with dexamethasone fully abolished the stress‐induced increase in adrenocorticotropin plasma level.Our results show that circulating corticosteroids reduce the stress‐induced activation of the medullary A1 and A2C2 groups i.e. those that contribute mainly to the catecholaminergic innervation of the hypothalamo‐pituitary‐adrenocortical axis within the hypothalamic paraventricular nuclei. However, since the feedback regulation of the central catecholaminergic systems is much less efficient than the feedback actually observed on the adrenocorticotropin secretion, we suggest that it is likely to play a minor physiological role in the overall feedback regulation exerted by circulating corticosteroids on the hypothalamo‐pituitary‐adrenocortical axis.
cFos Activity Identifies Recruitment of Luteinizing Hormone‐Releasing Hormone Neurons During the Ascending Phase of the Proestrous Luteinizing Hormone Surge
Authors: Lee Wen‐Sen , Smith M. Susan , Hoffman Gloria E. 
Published: September 2006

AbstractThe proto‐oncogene product of the c‐fos gene, cFos, is a useful marker for luteinizing hormone‐releasing hormone (LHRH) neuronal activation. While recent data indicate that in the rat, an LHRH surge plays an active role in stimulating the proestrous luteinizing hormone (LH) surge, the mechanics of the LHRH surge remain unknown. The aim of this study was to determine whether LHRH neuronal activation occurs entirely at the beginning of the LH surge or whether the number of LHRH neurons activated increases during the ascending phase of the surge. To accomplish this aim, we determined the relationship between the number of LHRH neurons expressing cFos and LH concentrations during the ascending limb of the proestrous LH surge. During the estrous cycle in the rat, on the afternoon of proestrus, the number of LHRH neurons expressing cFos increased as plasma LH levels increased to reach peak concentrations. The regression line describing these two variables had a very highly significant correlation coefficient, indicating a linear relationship. Treatment with RU486 to block progesterone's action on the afternoon of proestrus significantly reduced both the number of LHRH neurons expressing cFos and the magnitude of LH secretion during the entire ascending phase of the LH surge. An analysis of covariance with comparison of regression lines from untreated and RU486‐treated animals revealed that while both sets of data established significant linear relationships between the degree of activation of LHRH neurons and plasma LH values, the slopes of the two lines were different (P = 0.031) with no statistical difference in the two intercepts. These data, together with the demonstration of an overall reduction of cFos intensity following removal of progesterone's actions, suggest progesterone alters the dynamics of LHRH neuronal activation by significantly reducing the recruitment of LHRH neurons and suppressing the level of activation of individual LHRH neurons. The results of our study support the hypothesis that the ascending phase of the LH surge results from the gradual recruitment of LHRH neurons into the active state.
Acute Luteinizing Hormone and Prolactin Responses to Paced Mating Stimulation in the Estrous Female Rat
Authors: Erskine Mary S. , Kornberg Eva 
Published: September 2006

AbstractThe present experiments sought to characterize the particular stimuli received during mating in the female rat which induce acute increases in luteinizing hormone (LH) and prolactin (PRL) following copulation. Comparisons were made between cycling females mated on the evening of proestrus in partitioned chambers in which spontaneous patterns of approach/withdrawal toward the male served to pace copulatory stimulation (paced), in non‐partitioned chambers in which female regulation of intervals between copulatory mounts was prevented (non‐paced), or under conditions in which they received mounts‐without‐intromission (mounts‐only). Frequent blood samples were withdrawn via surgically implanted intra‐atrial catheters. In experiment 1, blood samples for LH determinations were taken at 15‐min intervals for 1 h prior to and for 2 h after mating on the evening of proestrus. In experiment 2, samples for PRL determinations were taken at 10‐min intervals for 30 min prior to and for 90 min after mating on proestrus and at 0300, 0400 and 0500 h on the day of estrus (reported times corrected for reversed light cycle). LH levels were significantly higher in paced animals 15 min after initiation of mating than in non‐paced and mounts‐only females; no differences in LH were seen between females who subsequently became or did not become pregnant/pseudopregnant (P/PSP). PRL values were not different between groups receiving the different mating treatments at any time; however, P/PSP animals showed significantly higher levels of PRL between 20 to 60 min after mating than did non‐P/PSP females. No differences in PRL were seen between mating treatments or pseudopregnancy condition at 0300 to 0500 h on estrus. Paced females in both experiments received intromissions at a significantly slower rate than did non‐paced females. There was a significant positive correlation (r = 0.619, P<0.001) between LH concentration at 15 min and the inter‐intromission interval (in seconds) in paced and non‐paced groups of females. These data suggest that an LH response to mating is dependent upon the particular characteristics of mating stimulation received. In addition, they demonstrate that PRL increases acutely after mating stimulation in animals destined to become P/PSP but does not increase in response to those characteristics of mating stimulation which induced increases in LH.
Characterization of Melatonin Binding Sites in the Pars Tuberalis of the European Hamster
Authors: Skene D. J. , Masson‐Pévet M. , Pévet P. 
Published: September 2006

AbstractMelatonin binding sites in the pars tuberalis of the European hamster (Cricetus cricetus) have been characterized using the radioligand 2‐[125I]iodomelatonin. Specific 2‐[125I]iodomelatonin binding was assessed using radioreceptor studies of pars tuberalis membrane preparations. Saturation studies revealed a single, high affinity site (Kd 39.8 (± 7.6 SEM) pM and Bmax 4.1 (± 0.5 SEM) fmol/mg protein, n=4). Kinetic experiments showed the 2‐[125I]iodomelatonin binding to be rapid, saturable and reversible. The Kd calculated from the dissociation and association rate constants was 19.4 pM. The order of potency of different indoles for inhibition of 2‐[125I]iodomelatonin binding was 6‐chloromelatonin > melatonin > 6‐hydroxymelatonin > N‐acetylserotonin > 5‐methoxytryptophol > serotonin > 5‐methoxytryptamine. GTP caused a dose‐dependent inhibition of the 2‐[125I]iodomelatonin binding. A saturation study showed that GTP reduced the number of binding sites by a third without altering their affinity. These results imply the presence of a G‐protein‐coupled melatonin receptor in the pars tuberalis of sexually active European hamsters.
Sexual Behavior Triggers the Appearance of Non‐Neuronal Cells Containing Gonadotropin‐Releasing Hormone‐Like Immunoreactivity
Authors: Silver R. , Ramos C. L. , Silverman A‐J. 
Published: September 2006

AbstractGonadotropin‐releasing hormone (GnRH) regulates the secretion of pituitary gonadotropins and facilitates the display of sexual behavior. We report that in doves, following a brief period of courtship, non‐neuronal cells containing GnRH‐like immunoreactivity (ir) are seen in the habenula of both male and female doves. These cells appear to be translocated from either the cerebrospinal fluid or from capillaries in the pia or choroid plexus into the parenchyma of the brain. Immunoreactive cells are virtually absent in the habenula in control animals housed alone. The identity of the ir cells that enter the habenula is unknown but they would appear to be of either the macrophage or the mast cell lineage. Both of these blood‐derived cells have heterochromatic nuclei and irregular cell surfaces with many filamentous processes, as do the GnRH‐ir cells. The vacuolated granules of the ir cells could be indicative of mast cell degranulation or of endocytic vesicles of a phagocytosing cell. These data suggest that there is a population of cells within the habenula that are of similar size and morphology to the GnRH‐ir ceils and are metachromatic when stained with toluidine blue. The latter is a property of heparin‐containing mast cells. Lineage specific markers that permit a double‐label study will be required to determine the exact nature of the GnRH‐ir cells. Whatever their lineage, the translocation of non‐neuronal cells into the undamaged adult central nervous system has not been described previously, and may provide a means of delivering biologically active substances into specific brain regions.
Interactions Between the Hypothalamo‐Pituitary Adrenal Axis and the Thymus in the Rat: A Role for Corticotrophin in the Control of Thymulin Release
Authors: Buckingham J. C. , Safieh B. , Singh S. , Arduino L. A. , Cover P. O. , Kendall M. D. 
Published: September 2006

AbstractOur recent observations in man suggested that the secretion of the thymic peptide, thymulin, is influenced by hormones of the pituitary‐adrenal axis. In the present study, we have used the rat as a model in order to examine 1) the effects of corticotrophin (ACTH) and glucocorticoids on the release of thymulin in vivo and in vitro, and 2) the influence of an acute rise in plasma thymulin on the secretion of corticosterone and luteinizing hormone.Immunoreactive thymulin was readily detectable in plasma from male Sprague‐Dawley rats(≃200 g). Chronic bilateral adrenalec‐tomy, which effectively removed endogenous corticosterone, produced highly significant (P<0.01) increases in the plasma concentrations of both ACTH and thymulin. Treatment of the adrenalectomized rats with dexamethasone, in a dose sufficient to suppress the hypersecretion of ACTH, maintained the plasma thymulin at a low level which did not differ significantly (P > 0.2) from that in sham‐operated controls.In vitro, two non‐specific depolarizing agents, K+ (56 mM) and veratridine (10 ≃M), caused significant (P<0.01) Ca2+‐dependent increases in thymulin release from segments of rat thymic tissue. Their effects were mimicked by ACTH1–39. The secretory responses to ACTH (0.025 to 1 ng/ml) were concentration‐dependent but a very high concentration (2 ng/ml) of the peptide was without effect. Dexamethasone (0.1 μM) reduced (P<0.05) the spontaneous release of thymulin in vitro but potentiated markedly (P<0.01) the secretory responses to ACTH (0.5 to 1.0 ng/ml).Administration of thymulin (0.1 and 10 μg/kg ip) produced, within 10 min, striking increases in the plasma thymulin concentration which were still evident at 30 min. The peptide concentration then declined rapidly and, within 24 h, was lower than that in the corresponding vehicle‐treated controls. The serum concentrations of corticosterone and luteinizing hormone were unaffected by the thymulin treatment. The saline vehicle (2.0 ml/kg ip) also produced a small increase in plasma thymulin concentration which was maximal at 10 min; a further small rise was evident 6 h after the injection but thereafter the thymulin values were indistinguishable from those in uninjected controls. A similar biphasic profile of serum corticosterone was apparent after the saline injection but the serum luteinizing hormone was unaffected.The results suggest that ACTH is a physiological enhancer of thymulin release and that, in certain circumstances, its effects may be potentiated by glucocorticoids.
Central Noradrenergic Lesion Impairs the Adrenocorticotrophin Response to Release of Endogenous Catecholamines
Authors: Al‐Damluji Saad , White Anne 
Published: September 2006

AbstractActivation of hypothalamic α1‐adrenoceptors stimulates the secretion of corticotrophin‐releasing factors which in turn stimulate pituitary adrenocorticotrophin (ACTH). This mechanism is important in the physiological control of ACTH secretion. This study assesses the feasibility of using the ACTH response to release of endogenous catecholamines as a means of detecting a hypothalamic noradrenergic lesion in vivo. Intracerebroventricular infusion of the catecholamine neurotoxin, 6‐hydroxydopamine, was used to destroy noradrenergic nerve endings in rats, with the purpose of producing a model that could be used to study alterations in ACTH responses that may result from a lesion involving central noradrenergic neurons. 6‐Hydroxydopamine (250 μg icv) significantly reduced hypothalamic noradrenaline content, indicating damage to noradrenergic nerve endings, without affecting postsynaptic receptor function, as judged by preservation of the effect of a selective α1‐adrenergic agonist. Pharmacological release of endogenous catecholamines, effected by combined administration of a catecholamine precursor and an α2‐adrenergic antagonist, stimulated the secretion of ACTH in control, but not in 6‐hydroxydopamine‐treated rats. Degeneration of hypothalamic noradrenergic nerve endings is not followed by denervation hypersensitivity, and is therefore accompanied by impairment of the ACTH response to release of endogenous catecholamines.
Arginine Vasotocin Gene Expression During Osmotic Challenge in the Chicken
Authors: Miihlbauer E. , Hamann D. , Xu B. , Ivell R. , Ellendorff F. , Grossmann R. 
Published: September 2006

AbstractThe avian hypothalamic nonapeptide arginine vasotocin (AVT) is released from axon terminals in the neural lobe upon the application of osmotic stimuli. We have investigated whether, and to what extent, hormone secretion from the neurohypophysis is related to gene expression in the hypothalamus. Results from hybridization experiments with an AVT‐specific cDNA probe indicate that in adult chickens stimulated by water deprivation or by hypertonic saline (2% w/v) drinking water, an upregulation of the AVT mRNA pool takes place, since consistently higher AVT mRNA levels compared to controls were monitored in osmotically challenged birds. This stimulatory effect was even visible at the transcriptional level after 19 h of water deprivation when osmolality was still near the basal value. In hens osmotically challenged by hypertonic saline drinking water for 5 days, a dissociation between osmolality and AVT plasma concentration was visible: extremely high plasma osmolality was accompanied by only moderately increased plasma AVT concentration. This might be caused either by exhaustion of stored hormone, or by downregulation of the system after chronic challenge. The latter suggestion is supported by the fact that the AVT mRNA concentration after 5 days of hypertonic saline challenge was well below the AVT mRNA levels of the groups with the more short‐term stimuli of water deprivation for 19 or 48 h. In 30‐day‐old chicks the hypothalamic AVT mRNA concentration hardly reached 70% of the adult value, although AVT plasma concentrations were similar to those in the mature bird.We conclude that osmotic challenge of the hypothalamo‐neurohypophysial system not only causes secretion of AVT from stores in the neural lobe but is accompanied by upregulation of AVT gene expression. Upregulation already occurs after marginal increase in plasma osmolality, as seen after 19 h of water deprivation in hens. In 30‐day‐old chicks gene expression is only slightly upregulated after short‐term water deprivation while increase in plasma AVT is even greater compared to hens.
Localization of Insulin‐Like Growth Factor‐II Receptors in Rat Brain by in vitro Autoradiography and Immunohistochemistry
Authors: Batch Jennifer A. , Werther George A. , Hogg Annette , Mendelsohn Frederick A. O. , Scott Carolyn , Oldfield Brian J. 
Published: September 2006

AbstractInsulin‐like growth factor‐ll (IGF‐II) and its receptor, which is homologous with the mannose‐6‐phosphate (M6P) receptor, are found in high levels in adult rat and human brain, though their role remains unclear. In order to point to possible regional functions, we have mapped and quantified IGF‐II/M6P receptors in sagittal sections of adult rat brain by in vitro autoradiography/computerized densitometry and immunohistochemistry. While in vitro autoradiography allowed mapping and quantitation, immunohistochemistry both confirmed mapping and allowed more detailed determination of cellular distribution of receptors. The two methods were generally in agreement with few areas of mismatching. By in vitro autoradiography, a discrete and characteristic distribution of IGF‐II receptor binding was demonstrated, with specific binding representing 85% of total binding. Displacement and specificity competition curves in arcuate nucleus and choroid plexus were typical for authentic IGF‐II receptors with half maximal displacement at 1 nM cold IGF‐II. IGF‐II receptor density, estimated by in vitro autoradiography, was very high in circumventricular organs, especially the median eminence, which had the highest binding in the brain. In the remainder of the brain there was concordance between the distribution of receptors identified by the two techniques, with greatest densities in the olfactory bulb and olfactory pathways, the hippocampus and discrete regions of the cerebral cortex, cerebellum, hypothalamus, thalamus and brainstem. There were however, some notable mismatches. Autoradiographic binding was high to very high in the median eminence, arcuate nucleus, suprachiasmatic nucleus and anterodorsal thalamic nucleus, whereas these areas were only poorly immunostained. Conversely, the septum showed moderate autoradiographic binding, but very prominent immunostaining of neurons in its dorsolat‐eral aspect. Using the immunohistochemical technique IGF‐II receptors were localized to specific neuronal groups such as the mitral cells of the olfactory bulb, Purkinje cells of the cerebellum and neurons in the red nucleus. Fibre pathways were not labelled by either technique.We conclude that IGF‐II/M6P receptors are widespread throughout rat brain, specifically in neurons and blood vessels, with a similar, but distinct distribution to IGF‐I and insulin receptors. Many of these regions have in common high rates of metabolic and synthetic activity, which may be mediated by IGF‐II/M6P and their receptors.
Norepinephrine Inhibits Vasopressin‐Stimulated Flank Marking in the Syrian Hamster by Acting Within the Medial Preoptic‐Anterior Hypothalamus
Authors: Whitman D. Carol , Hennessey Ann C. , Albers H. Elliott 
Published: September 2006

AbstractSyrian hamsters exhibit a form of scent marking behavior called flank marking. Flank marking, which is elicited during social contact with other hamsters and by the odors of other hamsters, communicates socially important information such as mate choice and dominance status. Vasopressinergic activity within the medial preoptic‐anterior hypothalamic continuum (MPOA‐AH) is essential for the expression of flank marking. In female hamsters, an inverse relationship exists between the expression of flank marking and sexual receptivity during the 4‐day estrous cycle. Since norepinephrine (NE) appears to facilitate sexual receptivity, the present study investigated whether NE might have an inhibitory effect on flank marking by acting on Vasopressinergic activity within the MPOA‐AH. Microinjection of 9.0 μM arginine vasopressin (AVP) into the MPOA‐AH stimulated high levels of flank marking. Microinjection of 9.0 μM AVP combined with NE in concentrations of 4.0, 0.4 or 0.2 nM, drastically reduced or eliminated flank marking. In contrast, AVP in combination with 0.09, 0.04 or 0.004 nM NE produced no significant reductions in flank marking. In addition, microinjection of 9.0 μM AVP, in combination with epinephrine (4.0 nM), but not dopamine (4.0 nM), serotonin (4.0 nM) or neuropeptide Y (900 μM), significantly reduced AVP‐induced flank marking. In male hamsters, microinjection of NE (4.0 nM) combined with AVP (9.0 μM) into the MPOA‐AH was not found to inhibit AVP‐stimulated flank marking. These results suggest that NE is involved in regulating the expression of flank marking during the estrous cycle by acting on Vasopressinergic activity within the MPOA‐AH.
Colocalization of Fos‐ and Glucocorticoid Receptor‐Like Immunoreactivities in the Rat Amygdaloid Complex After Immobilization Stress
Authors: Honkaniemi Jari , Fuxe Kjell , Rechard Leena , Koistinaho Jari , Isola Jorma , Gustafsson Jan‐Åke , Okret Sam , Pelto‐Huikko Markku 
Published: September 2006

AbstractIn the present paper we demonstrate the effect of immobilization stress on c‐fos‐like immunoreactivity (Fos‐LI) in the rat amygdaloid complex. Furthermore, since the subnuclei of the amygdaloid complex contain numerous glucocorticoid receptor‐immunoreactive (GR‐IR) neurons, we also studied the possible colocalization of GR‐ and Fos‐LI ie. Fos‐Lls and the action of a synthetic glucocorticoid, dexamethasone, and an anti‐glucocorticoid, RU 38486, on Fos‐LI. Immobilization stress caused a remarkable increase in the number of the Fos‐IR neurons in all the subnuclei of the amygdaloid complex except in the lateral nucleus. The majority of Fos‐IR neurons also contained GR‐LI, with the highest colocalization in the central amygdaloid nucleus. A similar induction of Fos‐LI after immobilization was seen in the hypothalamic paraventricular nucleus and almost all the Fos‐IR neurons in this nucleus also exhibited GR‐LI. Treatments with dexamethasone or RU 38486 prior to stress did not have any marked effect on Fos‐LI when compared to stress alone. The present findings suggest that Fos may function as a transcriptional regulator in the amygdaloid complex after stress and affect the synthesis of neurotransmitters and receptors in the amygdaloid neurons. Since we did not observe any effect of dexamethasone or RU 38486 on Fos‐LI, it is likely that glucocorticoids do not directly regulate the expression of the c‐fos gene or the formation of Fos protein. In view of the fact that Fos is capable of forming a stabile complex with GR and repress the transactivational capacity of GR, Fos may inhibit the negative feedback effect of circulating glucocorticoids and thus maintain elevated plasma glucocorticoid levels in stress.