摘要:

The influence of β-endorphin on the secretion of corticotrophin releasing factor (CRF) by isolated rat hypothalami in vitro was studied. β-Endorphin (10–11–10–10M) caused dose-related increases in the CRF contents of the hypothalami and of the medium in which they were incubated. Its effects were antagonized by naloxone (10–8–10–7M). In contrast, in higher concentrations (10–7–10–5M), it reduced, in a dose-dependent manner, both the spontaneous release of CRF from the hypothalami and the release which normally occurred in response to acetylcholine, 5-hydroxytryptamine, morphine, met-enkephalin and leu-enkephalin. The inhibition of CRF release was associated with a rise in the tissue content of the hormone and was not blocked readily by naloxone. The results support the concept that opioid substances may be involved in the control of hypothalamo-pituitary-adre

ISSN:0028-3835    

DOI:10.1159/000124266

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

To clarify the influence of primary testicular failure upon circannual hormone rhythmicity we have been studying, by cross-sectional design, 93 adult patients with Klinefelter’s syndrome (KS) and 64 adult healthy males to look for evidence of circannual rhythms in testosterone (T), LH, FSH and PRL plasma concentrations. Plasma samples were taken from 08.00 to 09.00 h and all hormones were measured by radioimmunoassay. The data were assessed by the single cosinor method in order to obtain evidence for any significant rhythm and to estimate its parameters mesor, amplitude and acrophase. In the controls, annual rhythms were validated for the secretion of T (annual crest time in September), LH (annual crest time in February) and FSH (annual crest time in January), whereas PRL did not show a significant annual rhythm. In KS, significant circannual rhythms were validated for the secretion of T (annual crest time in April) and FSH (annual crest time in September), but not for LH and PRL secretion. Our results suggest that in KS the circannual hormone rhythmicity may be influenced by seminiferous tubule dysgenesi

ISSN:0028-3835    

DOI:10.1159/000124267

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Neonatal administration of monosodium glutamate (MSG) to rodents results in severe damage to the arcuate nucleus of the hypothalamus (AN). MSG-induced AN damage produces profound alterations in hypothalamic neuro-transmitters and anterior pituitary function. Reproductive function is also severely compromised in both male and female MSG-treated rats. The present study investigated the developmental sequelae of MSG-induced alterations in hypothalamic monoamine metabolism as well as other aspects of MSG toxicity. Female rats given 4 mg/g of MSG on postnatal days 2 and 4 did not exhibit any significant alterations in hypothalamic monoamine metabolism on postnatal days 21 or 30, however, postpubertal MSG-treated females had significantly reduced levels of mediobasal hypothalamic (MBH) dopamine and DOPAC. In contrast, male MSG-treated rats had slight reductions in hypothalamic and MBH dopamine levels but these reductions were not statistically significant. Male MSG-treated rats did exhibit significant reductions in hypothalamic DOPAC on postnatal day 30 and MBH homovanillic acid (HVA) levels on day 100. Acetylcholine levels were also measured in the MBH and pituitary of adult male MSG-treated rats and found to be unaltered. The developmental profile of hypothalamic monoamines and their metabolites and MSG-induced alterations in dopamine and DOPAC levels in the MBH of female rats are discussed in relation to the neurochemical mechanisms involved in triggering puberty.

ISSN:0028-3835    

DOI:10.1159/000124268

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Recordings were made of single unit activity through chronically implanted electrodes within the hypothalamic paraventricular nucleus of freely moving male rats also bearing chronically implanted stimulating electrodes in the preoptic area (POA) and indwelling jugular cannulae. High frequency electrical stimulation of the POA evoked increases in the rate of electrical discharge in 58% of the units tested. Increases were recorded during each period of stimulation and were subsequently followed by a significant decrease in the rate of firing. In a substantial proportion of these neurones, bursting patterns of electrical discharge were observed before, during, and following stimulation of POA. When simultaneous removal of blood samples from these animals was performed, a significant increase in plasma corticosterone concentration, immediately following POA stimulation, was observed. The data obtained have provided a possible neurophysiological correlate of hypothalamic electrical activity that may be directly related to the neural control of adrenocortical secretion.

ISSN:0028-3835    

DOI:10.1159/000124269

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Plasma oxytocin-associated neurophysin concentration ([OT-RNP]) was used to evaluate the responsiveness of oxytocinergic neurons to an acute salt load in Long-Evans (LE) rats and Brattleboro homozygous (DI) rats. This responsiveness was compared with that of vasopressinergic neurons in LE rats as indexed by plasma vasopressin-associated neurophysin concentration ([VP-RNP]). Acute salt loading was induced by infusing 18% saline for 60 min into conscious, trained, chronically catheterized animals and plasma osmolality (Posm) and mean arterial pressure (MAP) were monitored. An increase in Posm was associated with a rise in [OT-RNP] and the relationship between Δ[OT-RNP] and ΔPosm was similar for both LE and DI rats over the first 40 min of infusion (21.6 and 19.7 fmol ml–1 mosm–1 kg–1, respectively). Although Posm continued to rise between 40 and 60 min infusion, [OT-RNP] actually fell slightly during this period in LE rats to a final elevation of 682 ± 40 fmol/ml above initial values whereas [OT-RNP] in DI rats continued to rise to a final elevation of 1,927 ± 288 fmol/ml above initial values at 60 min of infusion. The differences between these elevations at 60 min for LE and DI rats were highly significant (p < 0.001). For LE rats, the increase of [OT-RNP] with Posm for the first 40 min of infusion was much greater than the increase in [VP-RNP] with the slope between Δ[VP-RNP] and ΔPosm being only 8.3 compared to 21.6 fmol ml"1 mosm–1 kg–1 in the case of Δ[OT-RNP]. This difference was significant at p < 0.002. Of some additional interest was the unexpected finding that while MAP rose gradually with infusion of hypertonic saline in LE rats, it experienced a progressive decline during infusion in DI rats. The data obtained in this study indicate that oxytocin-producing neurons release more products than vasopressin-producing neurons in response to acute increases in Posm. In addition, functioning vasopressin-producing neurons may, either directly or indirectly, have some negative feedback influence on the release of oxytocin at high plasma osmolalities (ΔPosm between + 28 and + 40 mosm/kg FLO). Finally, the data on MAP imply that vasopressin-producing neurons may have a role in the hypertension that results from

ISSN:0028-3835    

DOI:10.1159/000124270

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

The effects of oxytocin (OT) on gonadotropin-releasing hormone (GnRH) release from the adult male rat mediobasal hypothalamus and median eminence were studied in an in vitro incubation system. OT induced a dose-related (10–13 to 10–9M) inhibition of both basal and KCl-stimulated GnRH release from the mediobasal hypothalamus. OT, but not arginine vasopressin, also inhibited GnRH release from the isolated median eminence, and this inhibition was blocked by treatment with an OT receptor antagonist. Moreover, antagonist alone stimulated GnRH release from the insolated median eminence. These results demonstrate that OT can inhibit in vitro release of GnRH by an OT receptor mediated mechanism at the level of neurosecretory terminals in the median eminence and suggest that the hypothalamic OT neuronal system may play an inhibitory role in the modulation of GnRH secret

ISSN:0028-3835    

DOI:10.1159/000124271

出版商:S. Karger AG    

年代:1986

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000124272

出版商:S. Karger AG    

年代:1986

数据来源: Karger