摘要:

Crude hypothalamic extracts prepared from brains of 1-day-old rats produced a dose-dependent inhibition of prolactin (Prl) release by adult male hemipituitaries, and to a lesser extent by hemipituitaries of adult ovariectomized (OVX), estrogen-primed rats. These extracts contained 6-fold lower levels of dopamine than adult hypothalami. The inhibitory effect of the adult hypothalamic extracts, contrary to infantile hypothalamic extracts could be blocked by spiroperidol. Digestion of the infantile hypothalamic extracts with pronase totally abolished their Prl release-inhibiting activity, indicating the peptidic nature of this inhibitory substance. In contrast to their effect on Prl release by hemipituitaries, infantile hypothalamic extracts stimulated Prl release from dispersed anterior pituitary cells of OVX estrogen-primed rats, pointing to the importance of estrogen in modulating prolactin release-inhibiting factor (PIF) activity and the possibility that the PIF receptor is trypsin-sensitive.

ISSN:0028-3835    

DOI:10.1159/000124623

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Effects of thyrotropin-releasing hormone (TRH) on growth hormone (GH) secretion were investigated in vivo (on intact or mediobasal hypothalamic lesioned rats tested under either anesthesia or free moving conditions) as well as in vitro (in incubation or perifusion systems of anterior pituitary tissue). The peptide induced a rapid, dose-dependent increase of plasma GH levels in free moving animals bearing an extensive lesion of the mediobasal hypothalamus including the median eminence. Under comparable conditions, TRH was ineffective in intact animals. After chloral hydrate anesthesia a GH response to TRH was recorded in both groups, but lesioned rats exhibited a better responsiveness to all doses tested. In vitro TRH increased GH release from incubated or perifused pituitaries sampled from both intact and lesioned rats in a transient and concentration-dependent manner. A similar effect was obtained with the (3 Me His2) analogue of TRH. These findings indicate that TRH can affect GH secretion at the pituitary level under specific experimental conditions and support the hypothesis that either peripheral hormones or other, still unidentified hypothalamic neurohormones may modulate this effect.

ISSN:0028-3835    

DOI:10.1159/000124624

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

The autoradiographic distribution of [3H]arginine vasopressin, [3H]spiperone, [3H]GABA, [3H]dihydroalprenolol and the peripheral-type benzodiazepine ligand [3H]Ro5-4864 were examined in the rat pituitary before and after pituitary stalk transection. Stalk transection produced dramatic changes in the cellular architecture of the pars nervosa. Glial fibrillary acidic protein, an astrocyte marker reported in pituicytes, increased after stalk transection, whereas neurofilament, a marker for neuronal innervation, was lost. These structural changes demonstrated a successful stalk transection, permitting interpretation of changes in the densities of several [3H]-ligands over the three lobes. [3H]Ro5-4864 binding was markedly increased, suggesting that this site was located on the pituicytes. Conversely [3H]spiperone and [3H]arginine vasopressin binding density over the pars nervosa decreased. In the mutant diabetes insipidus rat (Brattleboro), which lacks pituitary vasopressin, [3H]arginine vasopressin binding was undetectable in the pars nervosa. [3H]dihydroalprenolol and [3H]GABA binding sites were unchanged by the lesion. These results are discussed in terms of the occurrence of functional acceptors on pituicytes and their possible role in neurohydrophyseal secretions.

ISSN:0028-3835    

DOI:10.1159/000124625

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Many studies suggest that the hypothalamic opiate system modulates the secretion of LH and prolactin (PRL) by its effects on catecholamine release. We previously provided evidence that the LH response to the opiate receptor antagonist naloxone (NAL) may depend upon spontaneous activity in the hypothalamic noradrenergic system at the time the drug is administered. Thus, when NAL is given to rats which have low turnovers of hypothalamic norepinephrine (NE), only small transient rises in LH occur. This is contrasted to the effects of NAL on the LH responses of animals with high rates of NE turnover where marked amplification of phasic LH release is observed. In the present studies, we examined the effects of NAL on LH and morphine on PRL responses in androgen-sterilized rats (ASR). These animals do not respond to the positive feedback actions of estrogen by having LH surges, and hypothalamic NE turnovers do not increase during the afternoon as they do in normal rats. Female rats were given a single injection of testosterone propio-nate (50 µg s.c.) at 5 days of life and ovariectomized (OVX) at 100 days of age. Seven days later (day 0), estrogen capsules were inserted subcutaneously, and on day 2, their responses to NAL or morphine were examined. Comparable estrogen-treated gonadectomized controls also were studied. In control rats, NAL (10 mg/kg s.c.) markedly amplified the phasic secretion of plasma LH. In contrast, NAL had no effect on the basal afternoon secretion of LH in ASR. To determine if neonatal androgen treatment deleteriously affected opiate-tuberoinfundibular dopamine (TIDA)-serotonergic interactions, a second series of studies was performed. Estrogen-treated adult gonadectomized males, females and ASR were injected with morphine sulfate (10 mg/kg s.c). Blood was sequentially collected, thereafter, every 10 min for 70 min. Morphine produced a rapid rise in plasma PRL beginning within 10 min and peaking approximately 40 min after drug treatment. All 3 groups of rats secreted equivalent amounts of PRL, and no significant differences among the 3 groups were detected. We conclude that the failure of NAL to affect LH secretion in ASR is due to the permanent damage produced in the noradrenergic system by neonatal androgen treatment. The present data also demonstrate that prepubertal androgen treatment does not affect the ability of morphine to induce the release of PRL, an event thought to be mediated via interactions between the opiate, TIDA and serotonergic systems

ISSN:0028-3835    

DOI:10.1159/000124626

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Both opiates and serotonin (5HT) are known to inhibit LH release in ovariectomized rats, and estrogen has been shown to reverse certain serotonergic effects. Therefore studies were undertaken to compare the effects of morphine and the serotonin agonist 5-methoxy-NN-dimethyltryptamine (5MEODMT) on LH release in ovariectomized rats with and without estrogen priming. Serial blood samples were collected via jugular cannulae before and 5, 15, 30 and 60 min after intravenous administration of morphine, 5MEODMT or both to rats receiving no pretreatment, or a serotonin receptor antagonist (methysergide, METH; or ketanserin, KET) 60 min earlier. In the absence of estrogen, morphine inhibited LH release, and the response was delayed by METH or abolished by KET, suggesting mediation by serotonin2 (5HT2) receptors. 5MEODMT alone failed to alter the release of LH significantly, but apparently activated both stimulatory and inhibitory serotonergic systems. Blockade of 5HT2 receptors with KET enabled an inhibitory system to prevail. No significant changes in LH concentrations were observed following combined administration of morphine and 5MEODMT. Similarly, in estrogen-primed rats morphine appeared to activate both inhibitory (5HT2) and stimulatory (5HT1) systems, resulting in no net change unless the inhibitory system had been antagonized by KET. Administration of 5MEODMT alone or in combination with morphine resulted in a strong stimulatory effect which appeared to be mediated by 5HT1 receptors. These results suggest the existence of a multiplicity of serotonergic influences on the release of LH in the rat, not only in terms of particular species of 5HT receptors, but also in neuronal connectivity. Finally, it is clear that the responses to morphine and 5MEODMT are not only not equivalent, but are mediated by different mechanisms whose effects are integrated downstream in order to produce the observed effects on LH release.

ISSN:0028-3835    

DOI:10.1159/000124627

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

The tuberoinfundibular (A12) dopaminergic pathway, which originates in the arcuate and periventricular nuclei, is thought to play an inhibitory role in the regulation of episodic luteinizing hormone (LH) secretion. Neonatal treatment of rats with the neurotoxin monosodium-L-glutamate (MSG) causes extensive damage to the arcuate nuclei and up to 60% depletion of dopamine (DA) in the mediobasal hypothalamus. We hypothesized that such DA depletion should result in a hyperresponsiveness to subsequent administration of a DA agonist. To test this hypothesis, male rats were treated neonatally with MSG. Control rats received injections of equiosmotic saline. As adults the rats were orchidectomized and fitted with indwelling venous catheters. Blood samples were taken from these unanesthetized, unrestrained rats at 5-min intervals for a 1-hour period, at which time the animals received an intraperitoneal injection of one of the following drugs: apomorphine (0.8 mg/kg, a DA receptor agonist), bromocriptine (8.0 mg/kg, a DA receptor agonist), 0.9% saline (vehicle for apomorphine) or 95% ethanol (vehicle for bromocriptine). Blood sampling was continued for a further 2–2.5 h. Plasma LH was measured by RIA. Both apomorphine and bromocriptine produced striking inhibition of circulating LH levels in MSG-treated rats. Neither of the control treatments altered pulsatile LH secretion patterns. Administration of exogenous gonadotropin-releasing hormone produced LH peaks in all animals so treated, including those whose endogenous LH secretion had been inhibited by the DA agonists. These findings suggest that the depletion of DA induced by neonatal MSG treatment results in a supersensitivity to DA agonists. Furthermore, they support the theory that tuberoinfundibular DA is an inhibitory regulator of episodic LH secretion in the castrate rat, and that this inhibitory effect occurs at a suprapituitary sit

ISSN:0028-3835    

DOI:10.1159/000124628

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

β-Endorphin (βE) exerts a strong inhibitory action on plasma vasopressin (VP) of rats, after intracerebroventricular, but not after subcutaneous injection of the drug. This effect is time- and dose-dependent. Also in the water-deprived rat, this treatment leads to a strong decrease of plasma VP levels. When rats treated with histamine (HIS) intracerebroventricularly to stimulate VP levels are injected with βE to HIS treatment, βE partially prevents the increase of plasma VP levels. Naloxone subcutaneously administered, antagonizes the effect of βE in all the situations we investigated. Opioid receptors, located in the brain as well as in the pituitary, are possibly involved in these proce

ISSN:0028-3835    

DOI:10.1159/000124629

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

(125I-His1, D-Ala2, Nleu27)-growth hormone-releasing factor (GRF) (l-29)-NH2, initially developed as a possible radioligand for identifying GRF receptors in the anterior pituitary, was found to bind to rat hepatic membranes. The tracer was stable, bound rapidly and reversibly, and its dissociation was accelerated by GTP. Radioligand binding was enhanced by the divalent cations Mg2+, Ca2+ and Mn2+ and inhibited by the chelating agent EDTA. Vasoactive intestinal peptide (VIP), PHI, secretin, GRF(l-29)-NH2, (His1, D-Ala2, Nleu27)-GRF(l-29)-NH2, and (D-Ala2, Nleu27)-GRF(l-29)-NH2 dose-dependently inhibited tracer binding. The order of potency of the unlabelled peptides tested suggested that (123I-His1, D-Ala2, Nleu27)-GRF(l-29)-NH2 specifically identified a high-affinity subclass of VIP receptors in rat liver membranes.

ISSN:0028-3835    

DOI:10.1159/000124630

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

The purpose of this study was to define the vasopressin-sensitive area in the anterior hypothalamus-medial preoptic area (AH-MPOA) of the golden hamster that is involved in the expression of flank-marking behavior. Male hamsters implanted with guide cannulae stereotaxically aimed at various sites in the AH-MPOA were microinjected initially with 0.1 ng of arginine vasopressin (AVP) in a volume of 10 nl. Hamsters that flank-marked in response to these injections were subsequently microinjected into the same sites with kainic acid (0.2 µg/20 nl; n = 10) or an equal volume of 1 MNaOH as a vehicle control (n= 10). Four days later hamsters were tested for odor-induced flank marking by placing them into the recently vacated home cage of other hamsters and for flank marking in response to the microinjection of AVP. Animals treated with kainic acid exhibited significantly (p

ISSN:0028-3835    

DOI:10.1159/000124631

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Pituitary tissue contains phenol sulfotransferase (PST), the enzyme that catalyzes the sulfate conjugation of monoamine neurotransmitters. We carried out these studies with pituitaries obtained 21.3 ± 3.0 h postmortem (mean ± SEM; n = 21) to determine whether the biochemical properties and variations in levels of human pituitary PST activities were similar to those of PST in platelets from control subjects. PST in the human platelet has been studied thoroughly because of the possibility that platelet PST might reflect levels of PST activity in other tissues such as the pituitary and brain. Our results demonstrated 2 forms of the pituitary enzyme that were similar to the thermostable (TS) and thermolabile (TL) forms of platelet PST with regard to assay conditions, pH optima, Km values for multiple substrates, responses to 2,6-dichloro-4-nitrophenol (DCNP), and thermal stability properties. Pituitary samples also were obtained at autopsy 6.3 ± 0.33 h (mean ± SEM; n = 3) after death to determine the effects of storage at 4 °C on PST activities. After storage for 6–18 h, 83–99.6% of the TS PST activity remained and 44–66.9% of the TL PST activity remained. Pituitary TS PST activity in samples obtained within 12.1 ± 3.25 h after death was 121.0 ± 49.1 units/mg protein (mean ± SEM; n = 7) with a range from 9.7 to 367.6. TL PST activity was 35.6 ± 11.6 units/mg protein (mean ± SEM; n = 6) with a range from 6.1 to 80.7. Wide variations of both enzyme activities were also present in 3 pituitary tumor samples. Therefore, at least 2 forms of PST were present in the human pituitary, and the pituitary enzymes were biochemically similar to platelet TS and TL PST activities. It will now be feasible to determine whether variations in the levels of platelet PST activities might be useful measures of normal and tumor pituitary

ISSN:0028-3835    

DOI:10.1159/000124632

出版商:S. Karger AG    

年代:1986

数据来源: Karger