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ABSTRACT
Thyrotrophin-releasing hormone (TRH) stimulates GH secretion in domestic fowl by actions at pituitary and central nervous system sites. The possibility that this central action might be mediated by hypothalamic catecholamines or indoleamines was therefore investigated. When TRH was administered into the lateral ventricles of anaesthetized fowl the concentration of 3,4-dihydroxyphenylacetic acid (DOPAC, a metabolite of dopamine (DA)) in the medial basal hypothalamus (MBH) was increased within 20 min. The concentrations of MBH noradrenaline (NA), DA, serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were, however, unaffected by the intracerebroventricular (i.c.v.) administration of TRH, although the MBH concentrations of somatostatin and TRH were concomitantly reduced. A rapid increase in DA release into MBH extracellular fluid and its metabolism to DOPAC was also observed after i.c.v. or i.v. administration of TRH, in birds in which the MBH was perfused in vivo with Ringer's solution. Microdialysate concentrations of NA, 5-HT and 5-HIAA were not, however, affected by central or peripheral injections of TRH. Diminished GH responses to i.v. TRH challenge occurred in birds pretreated with reserpine (a catecholamine depletor), α-methyl-paratyrosine (a DA synthesis inhibitor) and pimozide (a DA receptor antagonist). These results therefore provide evidence for the involvement of a hypothalamic dopaminergic pathway in the induction of GH release following the central or peripheral administration of TRH. In contrast with its inhibitory actions at peripheral sites, DA would appear to have a central stimulatory role in regulating GH release in birds.
Journal of Endocrinology (1993) 138, 225–232
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The secretion of corticotrophin releasing activity (CRA) from the isolated rat hypothalamus incubated in vitro was investigated under various conditions of incubation and of pretreatment of donor animals providing hypothalami. Media from hypothalamic incubations were assayed for CRA by a validated double in-vitro bioassay technique which differentiates CRA from vasopressin.
A circadian rhythm was found in the secretion of CRA in vitro from isolated hypothalami obtained from animals killed at different times of the day. Secretion of CRA increased significantly at 19.00 h (dusk) compared with the secretion rate at 07.00 h, in synchrony with a rise in plasma corticosterone levels. In addition, both plasma corticosterone concentrations and CRA secretion in vitro were higher at 07.00 h than at 19.00 h after exposure of the donor animals to a reversed light cycle for 7–10 days.
Hypothalami obtained from animals chronically treated with betamethasone in the drinking water showed a diminished secretion of CRA in vitro. Exposure of untreated animals to ether vapour for 2 min immediately before death significantly increased the subsequent secretion of CRA in vitro. Ether exposure did not significantly affect the secretion of CRA in vitro from hypothalami of betamethasone-treated rats. There was a close correlation between plasma corticosterone levels and in-vitro CRA release after these treatments. The results suggest that the secretion of CRA examined in this way is a phenomenon which can reflect the changes which occur in the activity of the hypothalamo-pituitary-adrenal system in vivo during the 24-h cycle, after glucocorticoid treatment and after ether stress.
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ABSTRACT
Atrial natriuretic peptide, ANP(99–126), is derived from cardiac atrial tissue and has potent effects on salt and water homeostasis, including the inhibition of aldosterone and vasopressin release. Recent studies have also suggested that it may suppress the pituitary-adrenal axis. In addition, N-truncated forms of ANP, such as ANP(103–126), have been identified within the central nervous system, with a prominent hypothalamic localization in the paraventricular nucleus. We have therefore investigated whether ANP(99–126) and ANP(103–126) are able to modulate the release of the principal ACTH-releasing factor, corticotrophin-releasing factor-41 (CRF-41), from the rat hypothalamus in vitro.
The static incubation system has been previously described in detail. Male Wistar rats were decapitated between 09.00 and 09.30 h, their hypothalami rapidly removed, and four half-hypothalami incubated for 20-min intervals following a period of stabilization. The effect of the ANP peptides on the basal (B) and KCl (28 mmol/l)-stimulated (S) release of immuno-reactive CRF-41 was studied by means of successive incubations in the absence (B1, SI) and presence (B2, S2) of the peptides. The ratios B2: B1 and S2: S1 were compared with parallel control incubations by ANOVA.
Neither form of ANP had any effect on the basal release of CRF-41. ANP(99–126) caused a dose-dependent inhibition of CRF-41 release in the concentration range 1–100 nmol (P < 0·01). ANP(103–126) also suppressed the release of CRF-41 in the concentration range 100 pmol/l–100 nmol/l (P < 0·01), with a minimum S2:S1 ratio at 10 nmol/l, and a decrease in effect at 100 nmol/l. Finally, the stimulation of CRF-41 release induced by noradrenaline (10 nmol/l and 1 μmol/l) was non-competitively antagonized by 100 nmol ANP(99–126)/l and 10 nmol ANP(103–126)/l.
It was concluded that ANP may be an important regulator of the pituitary-adrenal axis by interaction with CRF-41. As there are data indicating that ANP may also directly inhibit the pituitary corticotroph, it would appear that central ANP is intimately involved in pituitary-adrenal function.
Journal of Endocrinology (1990) 126, 223–228
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ABSTRACT
The reproductive effects of placing micro-implants of melatonin in the mediobasal hypothalamus (MBH) and preoptic area (POA) were monitored in Soay rams. Groups of animals were initially conditioned to alternating 16 weekly periods of long days (16 h light:8 h darkness; 16L:8D) and short days (8L:16D) for at least 9 months to entrain the seasonal reproductive cycle. All experiments were then initiated at 10 weeks under long days when the animals were sexually inactive. In experiment 1, rams were exposed to short days for 14 weeks or maintained on long days to illustrate the photoperiodically induced re-activation and regression of the reproductive axis. In experiments 2–4, rams received micro-implants of melatonin in the MBH or POA, or received control treatments (sham-operated or no surgery) for 12–14 weeks while maintained on long days (total of 12 animals/treatment). The melatonin implants consisted of 22-gauge stainless-steel cannulae with melatonin fused inside the tip and were placed bilaterally in the brain. Incubation of the implants in Tricine-buffered saline (pH 8·0) at 37 °C showed that the release rate of melatonin was relatively constant after an initial peak in week 1 (means ± s.e.m.: 3·42 ± 0·43 μg/24 h).
Rams with melatonin implants placed in the MBH, but not in the POA, showed a consistently earlier re-activation of the reproductive axis compared with the control animals in all three experiments (12/12 for MBH vs 2/12 for POA). The mean time to maximum testicular diameter was 12·2 ± 0·9, 21·6 ± 1·8 and 22·3 ± 1·2 weeks for the MBH, POA and combined control groups respectively (MBH vs control, P < 0·01; analysis of variance). The premature growth of the testes in the MBH group was associated with an earlier increase in the blood plasma concentrations of FSH and testosterone, and the appearance of the sexual skin coloration. Removal of the implants resulted in a decline in all reproductive parameters. The melatonin treatments did not cause a detectable increase in the peripheral concentrations of melatonin, or affect the diurnal rhythm in melatonin which reflected the long-day photoperiod. When implants containing 125I-labelled melatonin were introduced into the brain the associated radioactivity was localized to within 1 mm of the implants.
The overall results demonstrate that the constant administration of melatonin into the MBH blocks the effect of the endogenous long-day melatonin signal and induces gonadal redevelopment. This provides the first evidence that melatonin acts within or close to the MBH to relay effects of photoperiod and influence the timing of the reproductive cycle in the ram.
Journal of Endocrinology (1992) 132, 201–215
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Abstract
Previous studies have shown that treatment with microimplants of melatonin in the mediobasal hypothalamus (MBH) of sexually inactive Soay rams exposed to long days induces an increase in the secretion of FSH and reactivation of the testicular axis, as normally occurs in response to short days. The current study was conducted to investigate the possible involvement of hypothalamic dopaminergic (DA) systems in this melatonin-induced effect. At 10 weeks under long days, sexually inactive Soay rams were treated in the MBH with micro-implants containing bromocriptine (DA agonist) or sulpiride (DA antagonist), given alone or in combination with melatonin, to establish whether the DA drugs would mimic or negate the effects of melatonin. All micro-implants were inserted bilaterally and left in place for 14 weeks; the study lasted a total of 28 weeks (14 weeks implant period and 14 weeks post-implant period) while the animals remained under long days. The ability of the micro-implants to release bromocriptine and sulpiride for 14 weeks was confirmed by incubating implants in vitro and testing for the presence of the compounds in the incubate using a pituitary cell bioassay. Profiles of FSH, determined in blood samples collected three times weekly, were significantly different among treatments (time × treatment interaction, P<0·001, ANOVA). Melatonin in the MBH induced a marked increase in the concentrations of FSH during the implant period, and a decrease during the post-implant period (P<0·001). Bromocriptine given alone in the MBH induced a decrease in the concentrations of FSH which became statistically different from the control during the post-implant period (P<0·05). Treatment with sulpiride alone also resulted in a suppressive effect during the post-implant period (P<0·01). When given in combination with melatonin, bromocriptine or sulpiride significantly reduced the melatonin-induced increase in the concentrations of FSH observed during the implant period (P<0·001). The results support the view that DA pathways in the MBH play an important role in the inhibitory regulation of gonadotrophin secretion in the ram. The inhibitory effect of bromocriptine is likely to result from the direct activation of the hypothalamic DA receptors linked to GnRH neurones regulating the secretion of FSH. The apparent paradoxical inhibitory effect of sulpiride is thought to be due to enhanced gonadal steroid negative feedback resulting from blockade of the inhibitory DA pathways, as evidenced by significantly increased secretion of testosterone (P<0·05) in the animals receiving sulpiride in combination with melatonin. The observation that DA drugs modified the effects of melatonin in the MBH provides evidence that hypothalamic DA pathways may participate in the mechanism by which melatonin mediates the effects of photoperiod on reproductive function in the ram.
Journal of Endocrinology (1995) 146, 543–552
Department of Neurosurgery, Farber Institute for Neurosciences, Thomas Jefferson University, 900 Walnut Street, Suite 400, Philadelphia, Pennsylvania 19107, USA
Department of Biology, Washington and Lee University, Lexington, Virginia 24450-03, USA
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Department of Neurosurgery, Farber Institute for Neurosciences, Thomas Jefferson University, 900 Walnut Street, Suite 400, Philadelphia, Pennsylvania 19107, USA
Department of Biology, Washington and Lee University, Lexington, Virginia 24450-03, USA
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Department of Neurosurgery, Farber Institute for Neurosciences, Thomas Jefferson University, 900 Walnut Street, Suite 400, Philadelphia, Pennsylvania 19107, USA
Department of Biology, Washington and Lee University, Lexington, Virginia 24450-03, USA
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Department of Neurosurgery, Farber Institute for Neurosciences, Thomas Jefferson University, 900 Walnut Street, Suite 400, Philadelphia, Pennsylvania 19107, USA
Department of Biology, Washington and Lee University, Lexington, Virginia 24450-03, USA
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Department of Neurosurgery, Farber Institute for Neurosciences, Thomas Jefferson University, 900 Walnut Street, Suite 400, Philadelphia, Pennsylvania 19107, USA
Department of Biology, Washington and Lee University, Lexington, Virginia 24450-03, USA
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Department of Neurosurgery, Farber Institute for Neurosciences, Thomas Jefferson University, 900 Walnut Street, Suite 400, Philadelphia, Pennsylvania 19107, USA
Department of Biology, Washington and Lee University, Lexington, Virginia 24450-03, USA
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number of ER-immunoreactive (ER-ir) cells in the ventromedial hypothalamus (VMH) and area lateral to it, and increases the number of ER-ir cells in the medial preoptic area (mPOA; Li et al. 1994 ) and parvocellular paraventricular nucleus (PVN
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implantation was performed under general anaesthesia, through a drill hole in the skull, in accordance with the stereotaxic co-ordinate system for sheep hypothalamus ( Welento et al . 1969 ) and procedure described by Traczyk & Przekop (1963) , positions
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SUMMARY
The protein, RNA and DNA content was measured in the pars distalis, hypothalamus and cerebral cortex of gonadectomized frogs (Rana esculenta) and compared with the levels in captive and in wild controls. Short-term (35 days) gonadectomy increased the weight of the pars distalis and also its RNA and protein content, whilst gonadectomy for a longer period (135 days, females only) depressed these parameters below control levels. In the hypothalamus, short-term gonadectomy increased the protein concentration, and long-term gonadectomy the RNA content. Captivity alone for 135 days caused a diminution in the weight and protein content of the pars distalis, although the various parameters showed an increase which correlated with the annual reproductive cycle. The DNA content (μg/mg tissue) of the pars distalis was similar in all groups suggesting that any weight changes were not due to changes in cell numbers. Neither gonadectomy nor captivity altered the nucleic acid and protein content of the cerebral cortex. The pars distalis weighed more in female frogs and contained more RNA and protein per mg.
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Angiotensin II exerts a potent dypsogenic stimulus on the hypothalamus, which contributes to its centrally mediated participation in the control of water balance and blood pressure. Repetitive intracerebroventricular (i.c.v.) injections of angiotensin II lead to a loss of effect characterized as physiological desensitization to the peptide's action. In the present study, we demonstrate that angiotensin II induces the expression of suppressor of cytokine signaling (SOCS)-3 via angiotensin receptor 1 (AT1) and JAK-2, mostly located at the median preoptic lateral and anterodorsal preoptic nuclei. SOCS-3 produces an inhibitory effect upon the signal transduction pathways of several cytokines and hormones that employ members of the JAK/STAT families as intermediaries. The partial inhibition of SOCS-3 translation by antisense oligonucleotide was sufficient to significantly reduce the refractoriness of repetitive i.c.v. angiotensin II injections, as evaluated by water ingestion. Thus, by acting through AT1 on the hypothalamus, angiotensin II induces the expression of SOCS-3 which, in turn, blocks further activation of the pathway and consequently leads to desensitization to angiotensin II stimuli concerning its dypsogenic effect.
Departments of, Physiology, Otorhynolaryngology, Department of Physiology, Section on Neural Gene Expression, Department of Cellular Neurophysiology, Department of Anatomy and Neurobiology, Molecular Neuroendocrinology Research Group, School of Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan
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Departments of, Physiology, Otorhynolaryngology, Department of Physiology, Section on Neural Gene Expression, Department of Cellular Neurophysiology, Department of Anatomy and Neurobiology, Molecular Neuroendocrinology Research Group, School of Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan
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Introduction The neurohypophyseal hormones arginine vasopressin (AVP) and oxytocin (OXT) are mainly synthesised in discrete groups of magnocellular neurosecretory cells (MNCs) that are located in the hypothalamus. The gene expression, synthesis and
