摘要:

The purpose of the present study was to assess whether the pineal-induced suppression of prolactin (PRL) cell activity in blind-anosmic (BA) rats was possibly mediated via the hypothalamic dopaminergic system. Prepubertal male rats were divided into the following groups: sham-operated (Sham), BA and blind-anosmic-pinealectomized (BAP). Animals from each group were sacrificed 1, 4 and 8 weeks after the operations. Blinding and anosmia resulted in pineal-dependent decreases in the weight of the testes, accessory organs and anterior pituitaries at 4 and 8 weeks but not 1 week after the operations. Likewise serum PRL levels were significantly decreased in BA rats at 4 and 8 weeks but this effect was not prevented in BAP rats. Hypothalamic dopamine (DA) turnover in BA rats at 1 week was twice that seen in either the Sham or BAP groups at that time; this effect ended by 4 weeks. There were no effects of any treatment on DA turnover at 8 weeks. Finally, PRL cell sensitivity to DA inhibition was determined by measuring the release of PRL from pituitaries incubated in vitro with either vehicle or 5 × 10–7M DA. None of the treatments caused significant alterations in the response to DA, though this must be interpreted with caution since only one dose of DA was used. From these data we conclude that: (1) there is an increase in DA neuron activity that precedes the inhibition of both PRL secretion and the reproductive system in BA rats, and (2) the inhibition of PRL cell activity in these animals is apparently not due to an increase in sensitivity to

ISSN:0028-3835    

DOI:10.1159/000124982

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Using indirect immunohistochemistry and an antiserum raised against rat corticotrophin-releasing factor (CRF) we have outlined an asymmetric network of cells and varicose fibers in sheep adrenal cortex. This network was not associated with the larger splanchnic nerves, but was occasionally found in small bundles or with blood vessels; in most instances fibers were found weaving independently through cortical parenchyma. A plexus of fibers was found in the zona reticularis, with a few fibers ramifying into adjacent medulla. Uni or bipolar cells were found throughout the cortex, with the greatest frequency at the corticomedullary junction; a multipolar-type cell was also found in this area. Staining of varicose structures and most cells was abolished by incubation with excess rat CRF 1–41, but not by ovine CRF or a range of other peptides. Though the immunoreactive species has not as yet been identified, it may thus share homology withsequences present in rat but not ovine CR

ISSN:0028-3835    

DOI:10.1159/000124983

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

The actions of opioids on electrically evoked release of oxytocin, vasopressin, and noradrenaline – using the [3H]-noradrenaline technique – from the rat neurohypophysis were examined in vitro. Antagonism of the action of endogenous neurohypophysial opioids with naloxone enhanced release of peptides and [3H]-noradrenaline differentially. Naloxone enhanced oxytocin release by 100 and 173% in two series of experiments (ED50 7× 10–7M), whilst vasopressin release was enhanced by only 30 and 20%, respectively. [3H]-noradrenaline release was maximally enhanced by 41% (ED50 2× 10–7M). We examined the opioid receptor subtypes mediating these effects using selective receptor agonists. The ĸ-agonist U-50,488H inhibited oxytocin and vasopressin release to a similar extent, but did not modify [3H]-noradrenaline release. The effects of U-50,488H were completely prevented by a tenfold molar excess of naloxone. The µ-agonist (Z)-Ala2, MePhe5 Gly-ol)-enkephalin also failed to inhibit [3H]-noradrenaline release and caused only a minor inhibition of oxytocin and vasopressin secretion. The δ-agonist (D-Pen2, D-Pen5)-enkephalin was without effect. We conclude that (1) ĸ-re-ceptors sensitive to U-50,488H mediate opioid inhibition of secretion from oxytocin and vasopressin nerve terminals; (2) when opioid actions are blocked by naloxone, opioid peptides within the neurohypophysis are shown to exert a much greater influence over oxytocin compared to vasopressin terminals; (3) neurohypophysial opioids also regulate release from noradrenergic terminals, although the nature of the receptors involved remains unclear, and (4) ĸ-receptors can mediate inhibition of neurohormone secretion by an action independent of the neurohypophysial noradrenerg

ISSN:0028-3835    

DOI:10.1159/000124984

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

The function of noradrenaline in the rat neurohypophysis was investigated by examining the effects of selective adrenergic receptor agents on electrically evoked release of oxytocin, arginine vasopressin, and noradrenaline using the [3H]-noradrenaline technique. Since endogenous opioids in the neurohypophysis suppress release of both neurohormones and of noradrenaline, we assessed the role of noradrenaline in mediating opioid actions on neurohormone secretion by examining modification of the action of the opioid antagonist naloxone by adrenergic receptor agents. The data suggest (1) that in addition to opioid receptors, ‘presynaptic’ α2receptors regulate release from neurohypophysial noradrenaline terminals; (2) noradrenaline released from neurohypophysial terminals acts on β- and α1-receptors to facilitate both oxytocin and arginine vasopressin release: this action only becoming evident at elevated levels of endogenous noradrenaline release attained following removal of presynaptic opioid or α2regulation, and (3) opioid peptides within the neurohypophysis act to inhibit oxytocin and, to a lesser extent, arginine vasopressin secretion, partly through inhibiting release of facilitatory noradrenaline. We propose a model in which opioids act in the neurohypophysis both independently of noradrenaline via ĸ-receptors on neurosecretory terminals or pituicytes and also via interaction with the noradrenalin

ISSN:0028-3835    

DOI:10.1159/000124985

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Corticotropin-releasing hormone (CRH) plays a key role in coordinating neuroendocrine, metabolic and behavioral responses in stress and affective disorders. To further investigate the effects of enhanced pituitary-adrenocortical activity upon sleep-related phenomena we administered four intravenous injections of 50 µg human (h)-CRH or saline to 11 normal males at 10 p.m., 11 p.m., 12 p.m. and 1 a.m. and measured plasma levels of cortisol and growth hormone (GH) as well as sleep EEG recordings throughout the night. Treatment with h-CRH resulted in a significant increase of mean (± SEM) cortisol secretion between 11 p.m. and 3 a.m. (h-CRH: 100.6 + 9.5 ng/ml; saline: 39.0 ± 1.5 ng/ml; p < 0.01). This initial cortisol increase after repeated h-CRH stimulations was followed by a period of attenuated plasma cortisol between 3 and 7 a.m. (h-CRH: 70.3 + 7.0 ng/ml; saline: 115.5 ± 8.0 ng/ml; p < 0.01). Cortisol surges after h-CRH were associated with a significant blunting of sleep-related GH release expressed as areas under concentration curves (h-CRH: 1.245 ± 0.32 ng/ml/min · 103; saline: 2.462 + 0.92 ng/ml/min· 103, p < O.01). In addition to these hormonal effects, h-CRH induced a decrease of REM and slow wave sleep (stages III and IV) while the amount of more shallow sleep (stages I and II)increased. These effects upon sleep structure were more pronounced during the second part of the night. We conclude that h-CRH induces effects in healthy humans (GH blunting and SWS reduction) which resemble those seen among hypercortisolemic depressives and surmise that CRH plays a role to mediate endocrine as well as behavioral phenomena in the affective dis

ISSN:0028-3835    

DOI:10.1159/000124986

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

A light and electron microscopic immunocytochemical study was undertaken to explore the fine structural organization of prolactin-immunoreactive axons in the rat median eminence. In adult intact males and females and in hypophysectomized females, light microscopic immunocytochemical labeling of the mediobasal hypothalamus revealed a marked concentration of prolactin-like immunoreactive fibers in the perivascular layer throughout the median eminence and the hypophysial stalk. At the electron microscopic level, immunostaining was associated with typical neurosecretory axons located either in the palisade layer where they displayed numerous contacts with tanycyte processes, or in the perivascular layer where they frequently contacted the perivascular space. Within the labeled axonal profiles, immunostaining was essentially located on secretory granules, 90–120 nm in diameter, whereas the microvesicles accumulated in some perivascular profiles constantly remained unlabeled. These data strongly suggest that most prolactin-immunoreactive axons of the median eminence release their content into the hypophysial portal vessels. In 1-day-old infant rats, intensely prolactin-like immunoreactive fibers were similarly localized in the most external layer of the median eminence, in which, contrary to adult animals, very slight if any tyrosine-hydroxylase-immunoreactive fibers were detected. Since earlier studies have provided evidence for a nondopaminergic prolactin-release-inhibiting factor in the hypothalamus of infant rats, and for an inhibitory effect of prolactin on pituitary mammotrophs, we propose that hypothalamic prolactin maycontribute, as an additional prolactin-release-inhibiting factor, to the multifactorial control of pituitary mammotroph

ISSN:0028-3835    

DOI:10.1159/000124987

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Congenitally hypogonadal (hpg) male mice are unable to synthesize biologically active gonadotropin-re-leasing hormone (GnRH). Implantation of normal fetal preoptic area tissue containing GnRH neurons into the third ventricle of adult hpg males significantly elevates pituitary levels of luteinizing hormone (LH) and corrects their hypogonadism. In all responding animals, immunoreactive GnRH neurons within the transplant innervate the median eminence of the host. To assess whether gonadal recovery in hpg hosts results from pulsatile secretion of GnRH from grafted neurons, we compared the pattern of variation in plasma LH levels in 19 hpg graft recipients with testicular growth to that of 10 normal adult mice. All animals were castrated prior to receiving an indwelling catheter in the jugular vein. Sequential blood samples were collected (t = 10 min) and assayed for LH. Pulsatile LH secretion was seen in 11 of 19 hpg hosts and in all control mice. While there was great variability between individual animals, measures of baseline LH, LH pulse amplitude and duration, interpulse interval, and LH pulse frequency revealed no difference between hpg graft recipients and normal castrates in their LH pulse pattern. Immunocytochemical analysis of the brain in hpg hosts suggested no correlation between any parameter of pulse activity and individual differences in GnRH cell number or GnRH fiber outgrowth into the median eminence. Sources of variation in LH secretion among graft recipients, and between hpg hosts and normal mice, are discussed. We suggest that transplanted GnRH neurons are capable of integration into a GnRH ‘pulse generator’ which can support a near-normal pattern of pulsatile LH secretion, leading to testicular growth and steroid product

ISSN:0028-3835    

DOI:10.1159/000124988

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Distribution and density of specific high-affinity 125I-neurotensin-binding sites were examined by light microscopic radioautography in the suprachiasmatic nucleus (SCN) of normal cycling, ovariectomized, or ovariectomized and estradiol-implanted female rats. In all three experimental groups, intense 125I-neurotensin labeling was detected within the ventrolateral component of the SCN. Whereas the topographic distribution and spread of the label was similar between each group, the density of the label was significantly higher (mean increase: 122%) in ovariectomized than in normally cycling females within the rostral third of the SCN. This effect was no longer apparent in females chronically implanted with estradiol at the time of gonadectomy. These results indicate that plasma gonadal steroids may regulate neurotensin receptors in the rat SCN. It is suggested that this mechanism might be implicated in the feedback control of gonadotropin and prolactin secretion.

ISSN:0028-3835    

DOI:10.1159/000124989

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

This study was designed to determine if norepinephrine (NE) stimulated release of pineal serotonin (5-HT) is receptor mediated and to identify the receptor(s) most influential in the release process. Efflux of 3H-5-HT from rat pineals in vitro was significantly increased within 5 min after NE was added to perifusion buffer in concentrations ranging from 0.1 to 3 µM3H-5-HT was not simply displaced from pinealocytes by NE, since buffer containing 3 µM 5-HT had no effect on 3H-5-HT efflux. Furthermore, NE enhanced 3H-5-HT secretion by a stereospecific process, since d-NE was significantly less effective than l-NE. The α1-adrenoreceptor agonists phenylephrine and cirazoline simulated the effects of NE, significantly increasing 3H-5-HT efflux in single and sequential stimulations. Furthermore, the α1-adrenergic receptor antagonist prazosin reduced NE-stimulated release of 3H-5-HT. In contrast, the α2- and β-adrenoreceptor agonists naphazoline or clonidine and isoproterenol, respectively, were without effect. In addition, the α2- and the β-receptor antagonists rauwolscine and timolol, respectively, had no effect on NE-stimulated release of pineal 5-HT. In conclusion, the data show that NE stimulates 5-HT release within minutes from rat pineal glands in vitro. Unlike the pineal mechanism controlling melatonin synthesis, which has a longer latency and requires β-adrenergic receptor activation, 5-HT release is regulated by activation of αi-receptors. Thus, the pineal may be useful model for studying how separate intracellular processes are controlled by common neura

ISSN:0028-3835    

DOI:10.1159/000124990

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

We have examined the effect of electrical stimulation in the subfornical organ (SFO) on the activity of neurons in the medial septum and diagonal band of Broca (MS-DBB) which project to the median eminence in the rat. Previous studies have suggested that septal neurons with such projections are luteinizing hormone releasing hormone neurons. Extracellular single-unit recordings were obtained from 69 neurons in the MS-DBB which were antidromically identified as projecting to the median eminence. Electrical stimulation (100–400 µA) in the SFO resulted in a relatively short-latency (22.8 ± 0.8 ms), short-duration (9.2 ± 0.8 ms) activation of 85% of 41 antidromically identified MS-DBB neurons tested. One neuron was inhibited by SFO stimulation, while the remaining 12% were unaffected. Stimulation in nearby regions, including the hippocampal commissure and paraventricular nucleus of the thalamus, failed to elicit a similar excitatory response from 19 identified MS-DBB neurons. These results identify a neuronal pathway between the SFO and septal neurons which project to the median eminence, supporting a possible role for the SFO in the control of luteinizing hormone releasing hormone release and hence gonadotropin secre

ISSN:0028-3835    

DOI:10.1159/000124991

出版商:S. Karger AG    

年代:1988

数据来源: Karger