摘要:

AbstractCentral oxytocin administration has a profound facilitatory effect on the patterning of the milk‐ejection reflex in the lactating rat. Lesion and microinjection studies indicate that this action is, in part, mediated via a population of limbic neurones in the bed nuclei of the stria terminalis and ventrolateral septum, which have been shown to possess oxytocin receptors and to be activated by selective oxytocin‐receptor agonistsin vitro.In vivoelectro‐physiological recordings reveal that some of these neurones display cyclical activity which is highly correlated to each milk ejection, and are rapidly activated following i.c.v. administration of oxytocin. coincident with the facilitation of milk ejection activity. A hypothetical model is proposed in which this population of limbic neurones serves to gate the activity of a pacemaker which, in turn, coordinates the bursting of hypothalamic magnocellular neurones. The oxytocin innervation of these neurones and their expression of oxytocin receptors increases in the post‐partum period, and the resultant enhanced sensitivity leads to a greater facilitatory response during lactation. Inhibitory opioid and noradrenergic inputs which converge on these oxytocin‐sensitive neurones may function to switch off the facilitatory circuit during periods of stress. Thus, this population of limbic neurones participates in the regulation of neuroendocrine activity during lactation by providing an appropriate degree of feedback to alter the patterning of the milk‐ejec

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1995.tb00661.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractEffect of different cytokines, human recombinant interleukin‐la and fl (IL‐1 a, 1L‐1 j), interleukin‐6 and tumor necrosis factor‐a (TNF) on adrenocorticotropin (ACTH) secretion was compared in sham‐operated rats and those with lesions of the hypothalamic paraventricular nucleus. IL‐1 a was less active than IL‐1 b in stimulating ACTH in sham‐operated rats. Intravenous injection of IL‐1 fl in sham‐operated animals resulted in a rapid elevation of ACTH secretion. Five days after surgical lesion of the paraventricular nucleus, the main hypothalamic source of hypophysiotropic corticotropin‐releasing factor‐41, the response to IL‐1 /I was attenuated but not abolished. This suggests involvement of extra‐paraventricular releasing factors in mediation of ACTH‐releasing activity of IL‐1 P, altered responsiveness of pituitary to CRFs, and/or direct action of IL‐1 j on the corticotrope cells. TNF resulted in a biphasic stimulation of ACTH concentration, with peaks at 15 min and 90 min. In paraventricular‐lesioned, TNF injected rats both of these ACTH peaks disappeared, suggesting that CRFs from the paraventricular origin mediates ACTH‐inducing activity of TNF. IL‐6 elevated ACTH secretion much later than the other intravenously injected cytokines, the peak was at 1 h in sham‐lesioned rats. Paraventricular lesion completely prevented the increase of ACTH plasma levels after IL‐6 injection. These data suggest that: (1) Effect of TNF and IL‐6 on hypothalamo‐pituitary‐adrenal axis is mediated through the hypothalamic paraventricular nucleus and (2) IL‐lB is able to r

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1995.tb00662.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractNeuroanatomical data have clearly demonstrated the existence of synaptic contacts between neuropeptide Y (NPY) endings and tuberoinfundibular dopaminergic (TIDA) neurons in the rat arcuate nucleus. In order to determine the influence of NPY in the biosynthesis of dopamine, we have studied the effects of NPY and some NPY analogs on tyrosine hydroxylase (TH) gene expression in TlDA neurons in the male rat. The following peptides: NPY, PYY, [Leu31, Pro34]‐NPY (a Y, receptor agonist) and NPY13–36(a Y2receptor agonist) were injected into the left lateral ventricle of adult male rats. All the animals were perfused with 4% paraformaldehyde 4 h after injection. Cryostat sections through the arcuate nucleus were processed for quantitative in situ hybridization. The intracerebroventricular injection of NPY, PYY and [Leu31, Pro34]‐NPY induced an increased of 43, 33 and 42%, respectively, in the number of grains overlying TH neurons. On the other hand, the Y2receptor agonist NPY13–36did not influence mRNA levels. These data then strongly suggest that NPY positively regulates the genetic expression of TH in rat TlDA neurons via the Y, NPY receptor

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1995.tb00663.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractLike neuronal cells, insulin producing cells (beta cells) possess nerve growth factor (NGF) binding sites and express mRNA coding for the low‐ and high‐affinity NGF receptors, p75NGFRand Trk‐A respectively. Although the role of NGF on neuronal cells is well documented, its function on beta cells is still unknown. As a first step towards the elucidation of the role of NGF on beta cells, we have characterized both types of NGF receptors on INS‐1 cells, a beta cell line derived from a rat insulinorna and studied some early post‐receptor events by comparing the signaling pathway of NGF in those cells and in PC12 cells, a well characterized NGF‐responsive cell line. By polymerase chain reaction, immunocytochemistry, cross‐linking and Western blot analysis, we clearly demonstrated that Trk‐A and p75NGFR, the two NGF receptors expressed in INS‐1 cells and PC12 cells are similar. Moreover, upon NGF treatment, Trk‐A is phosphorylated on tyrosine residues in both cell types in the same dose‐ and time‐dependent manner. These data clearly demonstrate that the first step of NGF signal transduction is similar in PC12 and INS‐1 cells. Although early responsive genes like NGFI‐A and c‐fosare induced in both cell types upon NGF treatment, the induction of c‐junexpression is restricted to PC12 cells. Furthermore, the expression of late responsive genes, such as vgf and transin, which are induced by NGF in PC12 cells, are not induced in INS‐1 cells. In conclusion, although the initial steps of NGF signal transduction are similar in PC12 and INS‐1 cells, some of the later differ. These dissimilarities could suggest that NGF plays different roles in

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1995.tb00664.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractAdministration of exogenous glucocorticoids is known to suppress the HPA axis and has been reported to occupy brain glucocorticoid receptors, eventually leading to down‐regulation. To determine the effects of chronic corticosterone administration on HPA axis function, corticosterone was administered as both 25% and 50% corticosteronekholesterol pellets. Rats were sacrificed 6 days after corticosterone pellet implantation. The 25% corticosterone pellets produced a small increase in morning corticosterone concentrations but no change in evening ACTH or corticosterone secretion. The 50% corticosterone pellets produced constant corticosterone concentrations of 5–6 pg/dl, with no circadian variation in corticosterone, indicating inhibition of evening ACTH and corticosterone secretion. The 25% corticosterone pellets produced no significant decrease in thymus weight or in adrenal weight; 50% corticosterone pellets produced significant decreases in thymus weight and adrenal weight. Neither 25% nor 50% corticosterone pellets produced significant decreases in GR in hippocampus and cortex. The 50% corticosterone pellets treatment resulted in a decrease in anterior pituitary POMC mRNA levels, a decrease in baseline and oCRH stimulated ACTH release from the anterior pituitary, and a near complete inhibition of the AM and PM response to restraint stress. These results suggest that: 1) the HPA axis was able to adjust to the small increase in glucocorticoids produced by the 25% cort pellets with minimal disturbances in function and 2) 50% corticosterone pellets exert a significant inhibitory effect on stress and diurnal ACTH secretion which appears to be exerted at the pituitary as well as possible inhibitory effects on br

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1995.tb00665.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractPituitary adenylate cyclase activating peptide (PACAP) is a member of the vasoactive intestinal peptide‐like peptide family. It is found in the hypothalamus, where the PACAP precursor is processed to form PACAP‐38, the C‐terminal truncated PACAP‐27 and PACAP related peptide (PRP). Both PACAPs are potent stimulators of anterior pituitary adenylate cyclase activity, but the physiologically relevant anatomical sources of PACAP and possible importance of PRP in this regard are poorly understood. Using immunocytochemistry with epitope‐specific antisera, we now show that PACAPS38, PACAP27‐ and PRP‐positive nerve fibres are all present in the rat median eminence. The major immunoreactive species present was PACAP38. Numerous PACAP38‐immmunoreactive nerve fibres were observed in the internal layer and a few were present in the posterior pituitary lobe. The external layer of the median eminence contained a few PACAP‐38‐immunoreactive fibres and PACAP‐38‐positive nerve terminals were rarely seen in the perivascular portal spaces. Surprisingly, delicate PACAP‐38‐positive nerve fibres were identified in the anterior pituitary lobe intermingled between the pituitary cells although none of the secretory pituitary cells contained immunoreactive PACAP38, PACAP27 or PRP and preproPACAP mRNA was not detected in the gland by Northern blotting or in situ hybridization. PACAP‐27‐ and PRP‐immunoreactive nerve fibres and terminals were found in the same locations as PACAP‐38 although generally in lower numbers. Specific radioimmunoassays and HPLC revealed that PACAP‐38 accounts for the vast majority of the adenohypophyseal PACAP‐immunoreactivity, whereas PACAP‐27 and PRP were found in low to undetectable concentrations. In primary cultures of rat pituitary cells and in the clonal gonadotrope‐derived aT3‐1 cell line, PACAP‐27 and PACAP‐38 were equipotent stimulators of cAMP accumulation, whereas PRP was ineffective. We conclude that the distribution of PACAP‐imrnunoreactive nerve fibres in the hypothalamus of the adult male rat is not that expected for a classic releasing factor suggesting that other sources of PACAP are relevant for stimulation of anterior pituitary cells or that the hypothalamic PACAP system is activated u

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1995.tb00666.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractNormonatremic and chronically hyponatremic rats were pretreated with naloxone (5 mg/kg) or isotonic (1 50 mM) NaCI, then were given i.v. injections of 2 M NaCl (2 ml) or were hemorrhaged (20 ml/kg). Baseline and post‐stimulus blood samples were withdrawn through indwelling jugular venous catheters. Baseline levels of plasma vasopressin (AVP) and oxytocin (OT) were similar in both normonatremic and hyponatremic rats and did not change after naloxone pretreatment. Increases in plasma AVP and OT levels in response to both hypertonic saline and hemorrhage were markedly blunted in the hyponatremic rats compared to the normonatremic rats. Naloxone pretreatment caused augmented AVP and OT secretion in response to hypertonic saline stimulation and hemorrhage in both the normonatremic and hyponatremic rats; the magnitude of the naloxone augmentations in the hyponatremic rats were sufficient to normalize the OT response to hypertonic saline and both the OT and AVP responses to hemorrhage. Our results therefore suggest that endogenous opioids are likely involved in the inhibition of stimulus‐induced AVP and OT release that accompanies chronic hypoosmolal

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1995.tb00667.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractIn rodents and rabbits, neuropeptide Y (NPY) has a bimodal effect on gonadotropin‐releasing hormone (GnRH) secretion. lntracerebroventricular (icv) administration or direct infusion of NPY into the median eminence (ime) suppresses GnRH release in ovariectomized (OVX) animals, but stimulates GnRH release in intact or OVX animals treated with ovarian steroids. Specific ovarian steroiddependent NPY effects are, however, not obvious in non‐human primates. In OVX rhesus monkeys, icv administration of NPY has been shown to suppress luteinizing hormone (LH) secretion whereas ime infusion of NPY stimulates GnRH pulses. In such animals, estrogen replacement does not reverse the inhibitory NPY effect on LH release, although estrogen enhances the stimulatory NPY effect on GnRH secretion. These observations led us to speculate that the bimodal NPY effects in non‐human primates may depend on either the site of NPY action or the nature of the steroid milieu. This study utilized the push‐pull perfusion (PPP) technique to examine the effects of either ime or icv infusion of NPY on GnRH release in OVX monkeys treated with or without both ovarian steroids. Without exception, irne infusion of NPY increased GnRH concentrations in push‐pull perfusates regardless of the steroid status of the animals. In contrast, GnRH levels were reduced during icv infusion of NPY in both untreated and estrogen/progesterone‐treated, OVX monkeys. These results indicate that, unlike other mammalian species, in the rhesus monkey the stimulatory and inhibitory effects of NPY on GnRH release depend on the site of NPY infusion within the brain rather than the ovarian steroidal

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1995.tb00668.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractThe present study was conducted to visualize neuropeptides in the SCN of a mustelid, the American mink in which seasonal cycles of reproduction rely totally on the annual changes in day length. At this time, data in mustelids are lacking. Results were obtained with in situ hybridization (ISH) using synthetic oligonucleotide vasopressin (AVP) and somatostatin (SOM) and with single and dual immunohistochemistry (IHC) performed with antisera against AVP, SOM, vasoactive intestinal polypeptide (VIP), gastrin releasing peptide (GRP) and met‐enkephalin (Met‐ENK) in untreated (AVP and VIP) or colchicine (SOM, Met‐ENK and GRP) treated adult male and female mink. The most striking result, evidenced by ISH as well as IHC was the lack of AVP, SOM and Met‐ENK immunoreactive (ir)‐neurons in the SCN. In contrast, strongly VIP ir‐perikarya were widely distributed within the SCN and gave rise to a dense network of fibres extending within the periventricular (peVA) and subparaventricular (subPVA) areas. Weakly GRP ir‐perikarya were also observed in the median part of the SCN. Dual IHC revealed that the magnocellular neurons located just dorsal to the SCN, in the peVA and subPVA co‐stored AVP with VIP, SOM or Met‐ENK. The lack of SCN AVP and SOM ir‐neurons, reported for the first time in a mammalian species, raises the question of their implication in the functions of the circadian pacemaker and its entrainment by the light/dark cycle in other species. The significance of the large neurons co‐storing peptides in the terminal field of VlPergic fibres originating in the SCN has also to be determined. These results suggest that VIP could be of major importance in processing photic information mediating circadian entrainment and conseq

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1995.tb00669.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:0953-8194    

DOI:10.1111/j.1365-2826.1995.tb00670.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY