摘要:

The role of endogenous opioids in the control of thyroid-stimulating hormone (TSH) secretion in uremic male rats was investigated using the narcotic antagonist naloxone. In order to eliminate the effect of weight loss due to uremia-induced anorexia as a cause of altered TSH secretion in uremia, we also studied a group of normal control animals who were pair-fed with the uremic animals, so that their weights were comparable to that of the uremic animals. Naloxone administration produced a significant increase in the basal concentration of TSH in the uremic rats, but had no effect on the baseline TSH concentrations in the other groups of animals. The peak TSH response to TRH (5 µg i.v.) was significantly blunted in the uremic animals compared to the normal controls and the starved animals. Naloxone administration did not alter the peak thyrotropin-releasing hormone (TRH) stimulated TSH response in any of the experimental groups of rats. Because of the possibility that the effects of naloxone on TSH secretion in the uremic rats were related to impaired clearance of the naloxone in those animals, an additional group of normal rats was given twice the dose of naloxone administered to the uremic animals. The higher dose of naloxone was similarly without effect on the basal or TRH-stimulated TSH secretion in this group. The data suggest that experimental renal failure is associated with diminished sensitivity of the thyrotroph to TRH stimulation and that this blunted sensitivity cannot be abolished by blockade of endogenous opioids by naloxone. Opioid blockade does, however, increase basal TSH secretion in uremic animals, suggesting an increase in endogenous opioidergic tone in uremia. The increase in TSH secretion following opioidergic blockade in uremic rats may be related to an increase in endogenous TRH secretion following opioid blockade

ISSN:0028-3835    

DOI:10.1159/000124911

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

The transient removal of dopamine (DA) selectively potentiated the prolactin (PRL) releasing action of thyrotropin-releasing hormone (TRH) but not vasoactive intestinal peptide (VIP). Consistent with these findings, the PRL-stimulating actions of agents which activated the Ca2+/protein kinase C second messenger pathway but not the adenylate cyclase system were also potentiated. In the current study we have extended these findings to determine the second messenger system mediating the potentiating action of the removal of DA. Dispersed anterior pituitary cells from E2-treated Sprague-Dawley rats were cultured on plastic coverslips. Cells tonically superfused with DA (500 nM were challenged with TRH (100 nM) 20 min after no additional treatment or a 10-min treatment with 8-Br-cyclic adenosine monophosphate (8-Br-cAMP), the Ca2+ ionophore A23187,12–0-tetradecanoyl-phorbol-13-acetate (TPA), TRH, or VIP. The potentiation of the TRH response was compared to the 4- to 5-fold potentiation observed following the removal of DA for 10 min. 8-Br-cAMP at the concentration used (500 µM) was unable to alter the basal rate of PRL release, but, as VIP (500 nM), potentiated 2- to 3-fold the PRL-releasing action of TRH. A prior administration of TRH (100 nM) did not affect the responsiveness of the cells to a second challenge with TRH 20 min later. Both A23187 (20 µM) and TPA (5 or 50 nM) induced a sustained rise in the rate of PRL release. TPA-treated cells showed an increased responsiveness to TRH, whereas A23187-treated cells did not. These results suggest that increasing cAMP levels either by VIP or 8-Br-cAMP in part mimics the potentiation caused by the transient removal of DA. Although TPA potentiated the PRL-releasing action of TRH, stimulating the influx of Ca2 + with the ionophore A23187 or the presumed activation of Ca2+/protein kinase C pathway by a priming treatment with TRH did not. Therefore, the mechanism by which TPA is potentiating the response to TRH is unclear. The finding that prior removal of DA or exposure to VIP can potentiate the action of TRH supports the concept that a secretory response can represent the integration of the action of multiple regulatory neurohormones delivered in a specific sequence, a so-called ‘pleotropic regula

ISSN:0028-3835    

DOI:10.1159/000124912

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

In order to ascertain the influence of gonadal steroid hormones on the secretory response of the hypothalamic-hypophyseal luteinizing hormone (LH) axis to acute stress, the effects of four specific stressors on LH release were compared in ovariectomized versus ovariectomized steroid-treated rats. Groups of adult female Copenhagen-Fischer 344 rats were ovariectomized for either 1 or 2 weeks and exposed for specific intervals to one of the following stressors: novel environment, strobe light, restraint, or swim. Additional groups of animals were ovariectomized for 2 weeks and injected with 10 µg estradiol benzoate 24 and 48 h prior to exposure to the same stress stimuli. Multiple blood samples were obtained from these and nonstressed experimental controls at specific time points before, during, and after stress exposure. Transfer of 1-week ovariectomized rats to a novel environment, followed by a return to their original quarters 30 min later, resulted in a well-defined pattern of increased LH release. Novel environment stress also stimulated LH release in 2-week ovariectomized rats, as indicated by the comparison of mean LH values from the pre-stress versus post-stress sampling periods by paired t test. Strobe light stress, on the other hand, had no effect on circulating LH in 1-week ovariectomized rats, but significantly increased mean post-stress plasma LH levels compared to mean pre-stress values in 2-week ovariectomized rats. While exposure to either 15 min of restraint or 10 min of swim stress had no effect on LH in rats ovariectomized for 1 week, both of these stressors resulted in a marked decline in LH release in 2-week ovariectomized animals. Circulating LH returned to pre-stress values by 45 min after initiation of restraint, but hormone levels remained suppressed after swim stress until the end of the experiment (60 min). The administration of naltrexone (NALT), an endogenous opiate receptor antagonist, effectively reversed the inhibitory effect of both restraint and swim on LH release in 2-week ovariectomized rats and resulted in a greater elevation in plasma LH in both groups of stressed rats compared to that observed in nonstressed NALT-treated animals. Ovariectomized estrogen-treated rats showed no alterations in LH release during exposure to either novel environment, strobe light, or swim stress. Restraint stress, on the other hand, resulted in a temporary, but significant elevation in circulating LH, detectable at both 10 and 25 min after onset of stress. Hormone values returned to pre-stress levels by 45 min after time zero. The results of the present study demonstrate that several acute stressors can elicit, under uniform experimental conditions, differential alterations in LH release and that these disparate hormonal responses may depend, in part, upon the animal’s gonadal steroid milieu. These findings suggest that specific stressors may influence LH release via individual mechanisms rather than a common pathway and support the view that gonadal steroid hormones fulfill an important modulatory role in the responsiveness of the hypothalamic-hypophyseal LH axis to a variety of acute stress stimuli. The current data also indicate that ovariectomy can result in time course related alterations in the LH response to specific stressors. From the present work, that NALT-induced reversal of the suppressive effect of both restraint and swim stress on LH release in 2-week ovariectomized rats suggests that endogenous opioid peptides may be involved in central inhibitory mechanisms activated by these two stressors in the gonadectomized anim

ISSN:0028-3835    

DOI:10.1159/000124913

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

A consistent group of gonadotropin-releasing hormone (GnRH) cell bodies occurs in the ventral hypothalamic tract at the infundibular lip (IL), just below the arcuate nucleus (ARC), at the site of the so-called GnRH ‘pulse generator’. Immunocytochemical studies were performed to examine contacts between these GnRH neurons and nearby opioid peptide (OP) neurons in the ARC. Vibratome sections of the medial basal hypothalamus were obtained from colchicine-treated, perfusion-fixed juvenile female rhesus macaques. They were sequentially immunostained for GnRH using the peroxidase antiperoxidase (PAP) technique and for adrenocorticotropic hormone (to identify OP neurons) using colloidal gold. The PAP and colloidal gold markers could be clearly differentiated at both the light and electron microscopic levels. OP+ and GnRH+ neuronal cell bodies occurred close together in the ARC-IL region, sometimes within the same electron microscope grid square. At the electron microscopic level, OP+ axons formed symmetrical synapses with GnRH+ somata and proximal axons, suggesting a pronounced inhibitory influence on GnRH neuronal activity. Examples of OPVGnRH+ axodendritic and dendrodendritic contacts were also observed. Furthermore, symmetrical synapses between GnRH+ axons and GnRH+ perikarya or dendrites were occasionally present. The data obtained here clearly indicate that direct OP inhibition of GnRH ‘pulse generator’ neurons occurs at the ARC-IL in juvenile primates. It is suggested that these OP neurons help mediate steroid-negative feedback at the hypothalamic level. Furthermore, it is suggested that OP/GnRH and GnRH/GnRH inhibitory contacts may play a role in maturation and control of reproductive f

ISSN:0028-3835    

DOI:10.1159/000124914

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

The effect of colchicine on the hypothalamo-neurohypophysial system of rats drinking 2% NaCl for 4, 6, or 90 days was investigated. Colchicine was injected at time 0 for the 4-day group and 48 h before sacrifice for the 6- and 90-day groups. Each experimental group was divided into two subgroups that were injected with 7 µg colchicine into either the cisterna magna or the lateral cerebral ventricle. The hypothalamo-neurohypophysial system was investigated immuno-cytochemically using an antiserum against both neurophysins (NPs) as primary antibody. The arginine vasopressin content of the neural lobe (NL) of rats salt loaded for 4 days and injected with colchicine on days 0 and 3 was determined by radioimmunoassay. The amount of immunoreactive NPs in the supraoptic nucleus, the paraventricular nucleus, and in the NL was decreased in salt-loaded rats. In salt-loaded rats injected with colchicine into the lateral ventricle, a substantially larger amount of immunoreactive NPs was present in these three areas. However, when colchicine was injected into the cisterna magna, only the supraoptic nucleus appeared loaded with immunoreactive NPs, while NPs were depleted from the paraventricular nucleus. In the NL of rats salt loaded for 90 days immunoreactive NPs were diminished markedly, and axon swellings (Herring bodies) had virtually disappeared. Colchicine treatment of these rats caused an increase of immunoreactive NPs in the NL approaching control values and a reappearance of a large number of axon swellings. Results similar to those obtained with immunohistochemistry for NPs were obtained when determining the arginine vasopressin content of the NL by radioimmunoassay. The present findings suggest that (1) the intracisternal and intraventricular administration of colchicine differentially affects the supraoptic and paraventricular nuclei; (2) colchicine treatment of chronically salt-loaded rats does not inhibit axonal transport of NPs, but blocks their release from axon terminals in the NL, and (3) the hypothalamo-neurohypophysial tract of salt-loaded rats is less affected by colchicine than that of nonstimulated animals

ISSN:0028-3835    

DOI:10.1159/000124915

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

The central part of the medial preoptic nucleus (MPNc), the encapsulated part of the bed nucleus of the stria terminalis (BSTe), and the posterodorsal part of the medial nucleus of the amygdala (MeAp) are all thought to be involved in the neural control of female reproductive behavior, as well as other neuroendocrine mechanisms. Although the developmental importance of gonadal steroids during the perinatal period on these sexual dimorphisms is well known, an understanding of possible activational effects on these cell groups of circulating gonadal steroids in the adult is less clear. In the present study we evaluated the number of cholecystokinin (CCK)-immunoreactive cells present within MPNc, BSTe, and MeAp of regularly cycling female rats over the estrous cycle. In addition, the effects of ovariectomy and estrogen replacement on CCK staining were also examined. The number of CCK-immunoreactive cells within each cell group varied over the estrous cycle with the fewest cells present in animals sacrificed while in diestrus. Proestrous female rats showed a greater number of cells within each nucleus, while intermediate numbers were found for animals in estrus. These changes appear to be due, at least in part, to changes in levels of circulating estrogen, since subcutaneous implants of estradiol prevented the decline in the number of CCK-stained cells within MPNc, BSTe, and MeAp that was seen in untreated, ovariectomized female rats. Thus, the present findings support the hypothesis that levels of CCK within cells of these three sexually dimorphic cell groups are regulated by circulating gonadal steroids within a physiologically relevant time frame and may possibly contribute to the activation of female reproductive behavior as well as other neuroendocrine functions.

ISSN:0028-3835    

DOI:10.1159/000124916

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Nuclear androgen receptors (Arn)were measured in the pituitaries and hypothalami of adult male golden hamsters which had been injected with a long-acting preparation of bromocriptine or had pituitaries from adult females transplanted under the renal capsules. Treatment with bromocriptine markedly reduced pituitary Arn and plasma prolactin levels without altering plasma testosterone levels or hypothalamic Ar N. Ectopic pituitary transplants did not affect Arn in either the pituitary or the hypothalamus. These findings suggest that normal rates of prolactin synthesis and/or secretion may be required for maintenance of Arn in the pituitary of adult male hamsters.

ISSN:0028-3835    

DOI:10.1159/000124917

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

The content of immunoreactive (ir)-β-endorphin, ir-dynorphin 1–17, and ir-dynorphin 1–8 was determined in hypothalamus, anterior pituitary, and neurointermediate lobe of rats 3–24 months of age. In the anterior pituitary ir-β-endorphin showed a progressive rise with age (0.5 ± 0.06 ng/tissue at 3 months to 1.02 ± 0.23 at 24 months); a similar change was seen in ir-adrenocorticotropic hormone content of the same tissues. No age-related change in neurointermediate lobe ir-endorphin content was observed. In the hypothalamus, the ir-β-endorphin content fell progressively from 3 to 18 months, but was restored at 24 months to levels indistinguishable from those at 3 months (16.2 ± 4.3 ng/tissue compared with 11.3 ± 4.0 at 24 months). The ir-dynorphin content did not change progressively over the age span examined, except in the case of anterior pituitary content of ir-dynorphin 1–17 which fell progressively between 3 and 18 months (from 1.65 ± 0.15 ng/tissue at 3 months to 0.73 ± 0.12). Radioimmunoassay following high-performance liquid chromatography analysis of extracts of the tissues showed little variation of the immunoreactive forms with age, with two notable exceptions. In the hypothalamic extracts from 24-month-old rats the ratio of the nonacetylated ir-endorphin to the acetylated ir-endorphin was lower than in equivalent extracts from 3-month-old rats. In anterior pituitary extracts from 3-month-old rats, ir-dynorphin 1–17 appeared as two peaks (putative 6K and 4K species) of approximately equal size. Between 3 and 18 months the smaller form became predominant, so that in extracts from older rats the larger form was not present. These results indicate that aging influences the net synthesis-secretion balance of these opioid peptides differently, between ages and between tissues. Finally, posttranslational processing of some of these peptides differs with age, as indicated by changes in immunoreactive forms observed on high-performance liq

ISSN:0028-3835    

DOI:10.1159/000124918

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

The objective of this study was to determine whether the negative feedback action of ovarian steroids on pulsatile luteinizing hormone (LH) release in the diestrous 1 (Dl)-diestrous 2 (D2) interval of the rat estrous cycle is mediated by endogenous opioid peptides (EOPs), by examining the pulsatile LH release response to naloxone infusions in the presence or absence of D1-D2 levels of estradiol (E2) and progesterone (P). As plasma E2 and P levels increased between Dl and D2, mean blood LH levels decreased due solely to a decrease in LH pulse amplitude as frequency remained stable. However, ovariectomy increased both parameters of pulsatile LH release, indicating the effect of loss of ovarian steroid-negative feedback in this interval. Replacement of D1-D2 plasma levels of E2 and P restored D2 values for both parameters of pulsatile LH release, and E2 + P did not alter in vivo pituitary responsiveness to LH-releasing hormone (LHRH). In ovariectomized rats lacking the negative feedback provided by E2 + P in this cycle interval, continuous infusion of naloxone caused a further dose-dependent augmentation in both LH pulse amplitude and frequency. This stimulatory action of naloxone was prevented by simultaneous infusion with morphine, and was not associated with any change in in vivo pituitary responsiveness to LHRH, indicating that this was an action exerted through centrally located EOP receptors. Naloxone also increased both parameters of pulsatile LH release in E2 + P-treated rats. However, the magnitudes of the naloxone-induced increments in LH pulse amplitude and frequency in ovariectomized, steroid-treated rats were not greater than those seen in ovariectomized, nonsteroid-treated rats given naloxone versus saline. In addition, mean values for both parameters of pulsatile LH secretion during EOP receptor blockade in steroid-treated rats were reduced when compared to values in ovariectomized, nonsteroid-treated rats infused with naloxone. Thus the stimulatory effect of naloxone on pulsatile LH release was similar in the presence or absence of the negative feedback action of D1-D2 plasma levels of E2 + P. This indicates that the negative feedback effect of E2 + P on pulsatile LH release in this interval is not mediated by EOPs whose actions are blocked by naloxone.

ISSN:0028-3835    

DOI:10.1159/000124919

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

In order to study the cellular and subcellular distribution of β-adrenergic receptors in the pars intermedia of the rabbit pituitary, we have developed a technique for the high-resolution radioautographic localization of β-adrenergic receptors, using [125]-cyanopindolol as the ligand. The most suitable fixative was the McLean fixative to which 0.1% glutaraldehyde was added. In semithin sections, specific labeling was localized over all the secretory cells. At the ultrastructural structural level, plasma membrane, nuclear envelope, and mitochondria appeared to be significantly labeled. These observations are consistent with previous results indicating the presence of β-adrenergic receptors at the level of the plasma membrane. On the other hand, the exact role of intracellular receptors remains to be clarified. Moreover, this technique which allows the localization of β-adrenergic receptors at the ultrastructural level should be very useful to study the distribution of these receptors in other tissues, especially the central nervous sys

ISSN:0028-3835    

DOI:10.1159/000124920

出版商:S. Karger AG    

年代:1988

数据来源: Karger