摘要:

Previous studies performed to elucidate an anterior pituitary site of action for β-endorphin (B-EP) in the regulation of prolactin (PRL) release have been inconclusive. The purpose of the present study was to further investigate if B-EP could stimulate PRL release by a direct action at the anterior pituitary. Anterior pituitaries from ovariectomized rats were dispersed, and the cells were plated in Ham’s F-10 medium. Following a 48-hour preincubation period, the effects of B-EP on basal PRL release and on the dopamine-inhibited PRL release were studied over a 24-hour period. Overall, B-EP at concentrations ranging from 10–8 to 10–6 M had no effect on basal release of PRL at 1, 3, 5 and 24 h, although a small but significant increase of 39% was observed with 10–6 M B-EP at 1 h of incubation only. B-EP at 10–6 M, but not at lower concentrations, significantly suppressed the inhibitory effects of 10–6 M dopamine on PRL release at 1 h but not at longer periods of incubation. Pretreatment of the cells for 3 h with 10–6 M naloxone completely antagonized the suppressive effect of B-EP on the dopamine-mediated inhibition of PRL release. Naloxone pretreatment of the cells had no effect on basal nor dopamine-inhibited release of PRL. Because of the high concentration of B-EP required to suppress the dopamine inhibition and the transitory nature of this B-EP effect, it is unlikely that the primary site of action for B-EP in regulating PRL release is at the anterior pituitary. However, high concentrations of B-EP may antagonize the inhibitory effect of dopamine on PRL release at the anterior pituitary through a specific opiate-medi

ISSN:0028-3835    

DOI:10.1159/000124028

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

The neurohypophysial nerve terminals of rats were studied by electron microscopy and morphometric analysis of vesicles and vacuoles labeled with horseradish peroxidase (HRP) after intraventricular injection of angiotensin II (AII). Exocytotic figures of neurosecretory granules from the nerve terminals were observed. The electron-dense materials resembling the contents of neurosecretory granules were occasionally observed in the extracellular spaces. A highly significant increase in the relative volume occupied by HRP-impregnated structures in the terminals occurred after administration of 500 ng AII These findings provide morphological evidence for the stimulation of neurohypophysial hormone secretion following administration of 500 ng AII

ISSN:0028-3835    

DOI:10.1159/000124029

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Urotensin I (UI), one of the biologically active peptides isolated from the caudal spinal cord and urophysis of fish, exhibits a strong sequence homology with mammalian corticotropin-releasing factor (CRF). We have applied an antiserum to ovine CRF that cross-reacts completely with UI to sections taken from the caudal spinal cord and urophysis of the channel catfish (Ictalurus punctatus). Using the indirect immunofluorescence technique, the presence of striking Ul-like immunoreactivity was observed within discrete neuronal structures. UI immunoreactivity was found within large-diameter neuronal perikarya in spinal cord segments immediately rostral to the urophysis, in fascicles of nerve fibers as the urophysis emerges, and in a dense plexus of nerve fibers and terminals which abut capillary loops within the urophysis. The localization of UI immunoreactivity within discrete neurosecretory neurons of this system will make it possible to more fully determine the nature of the regulatory mechanisms controlling its secretion.

ISSN:0028-3835    

DOI:10.1159/000124030

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

The effect of altering γ-aminobutyric acid (GABA) activity on growth hormone (GH) secretion of freely moving chronically cannulated male rats was studied. Systemic injection of the GABA agonist muscimol (2 mg/kg i.v.) inhibited the anticipated secretory episode. Increasing brain GABA levels by γ-acetylenic-GABA (50 mg/kg i.v.) also inhibited the expected GH rise. When injected before the expected secretory episode, the GABA receptor antagonist bicuculline methiodide (2 mg/kg i.v.) triggered an early secretory peak. GABA and muscimol failed to change GH secretion by cultured anterior pituitary cells. When the somatostatin input to the stalk-median eminence region was interrupted by an anterolateral cut around the medial basal hypothalamus, the GH level was steadily increased and muscimol injections caused a prompt decrease of plasma GH levels. These results are consistent with the hypothesis that GABAergic tonic inhibition participates in the control of GH secretion and that GABA inhibits spontaneous GH release by inhibiting the secretion of a GH-releasing facto

ISSN:0028-3835    

DOI:10.1159/000124031

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Pulsatile secretion of luteinizing hormone (LH) in ovariectomized rats was evaluated before and after local implantation of crystalline estradiol benzoate (EB) into various regions within the forebrain. Serum concentrations of LH were measured by radioimmunoassay in samples collected at 6-min intervals through indwelling cardiac catheters. In rats with EB implanted in the preoptic suprachiasmatic area (POSC), and in the nucleus of the tractus diagonalis and the diagonal band of Broca (DBB) to a lesser extent, the mean LH concentration and LH pulse frequency decreased rapidly while the pulse amplitude did not change for 3 h after implantation. Rats with the EB implant in the bed nucleus of stria terminalis, the medial preoptic area, the medial septal nucleus, the anterior hypothalamic area or the third ventricle showed unchanged frequencies of LH secretory pulses. Implantation of progesterone into the POSC of ovariectomized rats produced no significant change in LH secretory profiles. It was suggested that the sites of action of estrogen in decreasing the LH pulse frequency are not widespread but rather restricted within a small part of the brain, including the POSC and DBB, in the ovariectomized rat.

ISSN:0028-3835    

DOI:10.1159/000124032

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

A new method for estimation of in vitro neurosecretory activity of tuberoinfundibular dopaminergic (TIDA) neurons was developed by measuring the rate of synthesis of dihydroxyphenylalanine (DOPA) in the median eminence of hypothalamic slices. Sagittal hypothalamic slices of ovariectomized rats were incubated in a medium containing 3-hydroxybenzylhydrazine (NSD 1015), an inhibitor of DOPA decarboxylase. DOPA accumulated in the median eminence following incubation with NSD 1015 was determined by high-performance liquid chromatography with electrochemical detection. The amount of DOPA accumulated in vitro in the median eminence was maximal in a medium containing 10 mM NSD 1015 and linear up to 120 min at 37°C. Increasing the concentration of tyrosinein medium stimulated the synthesis of DOPA in the median eminence. The synthesis of DOPA was blocked by 1 mM α-methyltyrosine, an inhibitor of tyrosine hydroxylase. The rate of in vitro synthesis of DOPA in the median eminence was 33% of that of in vivo synthesis. Incubation in a medium containing 50 mM K+ to depolarize neurons caused a 2.4-fold increase in DOPA synthesis in the median eminence. The high K+-induced increase in DOPA synthesis was blocked by omission of Ca2+ and addition of 1 mM EGTA into the medium, suggesting Ca2+ dependency of depolarization-activated DOPA synthesis. These results indicate that this in vitro assay is a useful means to study the regulatory mechanisms of TIDA neuron

ISSN:0028-3835    

DOI:10.1159/000124033

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

In man and other mammals, starvation is accompanied by a severe suppression of luteinizing hormone-releasing hormone (LHRH) and luteinizing-hormone (LH) secretion, which is caused by unknown alterations in hypothalamic functions. Prostaglandin E2 (PGE2), endorphins and testosterone (T) are know to be strongly involved in the regulation of LHRH release. The present study examined whether the influence of these substances on LHRH and LH secretion was affected by starvation. In vitro experiments checked the release of PGE2 and LHRH from median eminences (ME) of fed male rats and ones starved for 5 days. Stimulation with potassium (80 mM) induced an equally strong release of PGE2 and LHRH from the MEs of both fed and starved rats. When PGE2 (10 4M) was added to the superfusion medium, the potassium-stimulated release of LHRH was significantly enhanced in both groups of animals. The results clearly showed that in the terminal region of the hypothalamic LHRH system the release of this hormone and the action of PGE2 were not altered by starvation. In vivo experiments tested whether the effects of LHRH, PGE2, naloxone (NAL), or T on LH secretion were different in intact or castrated male’rats fed or starved for 3 and 5 days. LHRH (250 ng/kg) stimulated the same amount of LH secretion in fed and starved rats. The starvation-induced LH suppression was not due to a dysfunction at the pituitary level. The stimulatory action of PGE2 (1 mg/kg) on LH was gradually reduced throughout the starvation period. NAL (5 mg/kg) had little, respectively, no effect on LH release on the 3rd or 5th day of starvation. When given simultaneously, NAL did not affect the action of PGE2 in any of the three nutritional states. The interference of factors other than endorphins or PGE2 is assumed for starvation-induced suppression of LH secretion. Starvation did not alter the influence of T (ca. 3 ng/ml plasma) on LH secretion at the pituitary level. The stimulatory effect of PGE2 on LH release was completely suppressed by T in fed, as well as in castrated rats starved for 3 or 5 day

ISSN:0028-3835    

DOI:10.1159/000124034

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

We studied the effect of aging on vasopressin (VP) release from isolated neurohypophyses (NH) individually superfused with synthetic medium TC 199 with Hanks’ salts. The superfusion technique is described in detail. Male Fisher 344 rats 2 months (young, n = 17), 12 months (adult, n = 14) and 30 months (old, n = 17) of age were used. VP was measured by radioimmunoassay (RIA). The age-related VP release was analyzed as follows: initial traumatic release, basal release, VP release evoked by electrical stimulation (10-second trains every 20 s of matched biphasic stimuli, 0.2 ms width, 8 mA, 30 Hz), by chemical stimulation (56 mM K+) and total release for the entire superfusion period. When VP release was expressed per milligram NH, it was significantly lower under all conditions in the old rats than in the young ones. In the adult rats, traumatic, basal and total release values were similar to those of the young rats, whereas their responses to chemical and electrical stimulation were similar to those of old rats. Residual VP content expressed per whole NH was significantly higher in the old and adult rats, reflecting a larger glandular size, but when expressed per milligram NH tissue, it was low in the old rats. The percent of VP released during the entire superfusion period relative to the residual VP content was significantly lower in the old than in the young and adult rats. The magnitude of the maximal VP release exceeding the basal release, in response to electrical and chemical stimulation, was similar in young and old rats. However, in the adult rats it was significantly lower than in both the young and old following chemical stimulation. A significantly larger number of old and adult NHs exhibited a more delayed response to chemical, but not to electrical stimulation, than did the young NHs. These data demonstrate an age-related decrease in VP release in Fisher 344 rats. Since the traumatic and basal VP release in the adult rats is similar to the release in the young rats, while the stimulated release in the adult rats resembles the response of the old animals, the results suggest that an impairment of stimulated VP release occurs at an earlier stage of the aging process than does an impairment of spontaneous (traumatic and basal) releas

ISSN:0028-3835    

DOI:10.1159/000124035

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

The purpose of these experiments was to determine whether daily gonadotropin surges that occur in intact or ovariectomized hamsters kept in short days (less than 12 h of light/day) are manifest because of extremely low levels of steroids. Hamsters were ovariectomized and placed in l6L:8D or lOL:l4D. After 10–13 weeks, animals in each photoperiod were divided among four treatment groups: (1) estradiol implant plus progesterone injection 5 days later; (2) estradiol implant plus water injection; (3) empty implant plus progesterone injection; (4) empty implant plus water injection. Blood samples were taken from animals in the morning and afternoon before and after various treatments. In animals not receiving estradiol, all short-day and some long-day females showed low morning values of LH and surge values in the afternoon. Estrogen suppressed morning and enhanced afternoon values of LH in long-day animals, intensifying the surge. However, in the presence of estrogen, these LH surges eventually diminished in both photoperiods. Progesterone hastened the loss of the LH surge. Hamsters did not consistently demonstrate FSH surges until treated with estrogen. Serum FSH in untreated hamsters was much higher in long-day than in short-day animals. Treatment with both steroids maximally suppressed morning and afternoon FSH levels in all hamsters. Thus, in the absence of estrogen, circadian expression of LH surges always occurs in short days; FSH surges sometimes occur. In all animals showing spontaneous or estrogen-induced surges, estrogen eventually leads to inhibition of gonadotropin secretion, particularly in the presence of progesterone. The data suggest that during anestrus caused by short days, the very low levels of estrogen in intact hamsters is permissive for circadian LH secretion which may be involved in the etiology of anestru

ISSN:0028-3835    

DOI:10.1159/000124036

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

The sexual behaviour of male rats, castrated and testosterone-implanted, declined following induction of hyperprolactinaemia by domperidone. Treatment with oestradiol benzoate did not reverse this effect, and may have accentuated it. Oestradiol also amplified domperidone-induced hyperprolactinaemia. Testosterone or dihydrotestosterone (DHT) apparently delayed, but did not prevent, the gradual deterioration in sexual behaviour (prolonged ejaculation latencies) induced by domperidone, but this effect was not confirmed statistically. Adrenalectomy, followed by cortisol replacement, failed to prevent the behavioural effects of hyperprolactinaemia. No consistent changes in serum progesterone or corticosterone could be found in hyperprolactinaemic rats in which the adrenals had not been removed. In vitro formation of DHT from precursor testosterone was reduced in the amygdalae of hyperprolactinaemic rats, but not in the hypothalamus or caudal spinal cord. Oestradiol cytosol binding was unchanged in all brain areas, except for a small but significant increase in the anterior hypothalamus. These results do not support a role for altered adrenal activity in determining the effects of high levels of prolactin on sexual behaviour. There is evidence for an impaired formation of DHT in the brain, but this may account for only part of the behavioural changes observed. It is possible that the major effect of prolactin lies in neural systems directly responsive to it, rather than in altered steroid secretion or metabolism.

ISSN:0028-3835    

DOI:10.1159/000124037

出版商:S. Karger AG    

年代:1984

数据来源: Karger