摘要:

Day length regulates the negative feedback potency of gonadal steroids upon luteinizing hormone (LH) in seasonal breeders such as the golden hamster. We have used an exchange assay employing 3H-R1881 to determine whether nuclear androgen plus receptor levels in the preoptic area, medial basal hypothalamus, or anterior pituitary differ between male hamsters maintained in long or short days. Cell nuclear androgen plus receptor levels in brain and anterior pituitary were significantly lower in intact males maintained in short days; these differences reflected significant decreases in testis size and serum testosterone (T) levels upon exposure to inhibitory photoperiods. In castrated males in which serum T levels were ‘clamped’ by the insertion of T-filled Silastic capsules, exposure to short days was not correlated with an increase in preoptic area, medial basal hypothalamus, or anterior pituitary receptor occupancy even though T’s negative feedback actions upon LH were clearly enhanced. In contrast, there were instances in which androgen receptor occupation was elevated in males exposed to long days. Our results suggest that in the male golden hamster, the well-documented increase in the ability of T to suppress LH secretion in short photoperiods cannot be attributed to an increase in receptor-mediated uptake and nuclear accumulation of androgen in target cells in the brain and anterior pituitary

ISSN:0028-3835    

DOI:10.1159/000124892

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Histamine (HA) is likely to participate in the neuroendocrine regulation of prolactin (PRL) secretion. We, therefore, studied the possible involvement of HA in the stress-induced release of PRL in conscious male rats. HA (30 µg) infused intracerebroventricularly 15 min before decapitation elevated PRL plasma levels from 5 + 1 to 54 ± 6 ng/ml (p < 0.01). Intracerebroventricular infusion of the H2 receptor antagonists cimetidine (CIM; 100 µg) or ranitidine (RAN; 125 µg) abolished the PRL response to HA (p < 0.01), while intracerebroventricular infusion of the H1 receptor antagonist mepyramine (MEP; 100 µg) inhibited the response only 40% (p < 0.05). Intra-arterial infusion of CIM (2,000 µg) or RAN (2,500 µg) inhibited the HA-stimulated PRL secretion 52% (p < 0.01) or 63% (p < 0.01), respectively. The H1 receptor antagonists MEP (1,000 µg) and SKF-93944 (1,500 µg) had no effect following intra-arterial administration. Restraint stress increased the PRL level to 84 ± 6 ng/ml (p < 0.01 vs. control). This effect was prevented by intracerebroventricular infusion of CIM or RAN (p < 0.01) and inhibited 75% by MEP (p < 0.01). Intra-arterial infusion of CIM, MEP, and SKF-93944 inhibited the stress response about 50% (p < 0.01), while RAN decreased the response only 25% (p < 0.05). Ether stress elevated the plasma PRL concentration to 46 ± 5 ng/ml (p < 0.01 vs. control). When infused intracerebroventricularly, CIM or RAN prevented the response (p < 0.01), while MEP had no effect. Intra-arterial infusion of CIM or RAN attenuated the response approximately 50% (p < 0.01), while intra-arterial infusion of MEP or SKF-93944 inhibited the response 80% (p < 0.01). We conclude that restraint as well as ether stress stimulates the secretion of PRL via release of neuronal HA. The effect of HA seems primarily mediated through activation of H2 receptors, whereas H1 receptors appear to play a

ISSN:0028-3835    

DOI:10.1159/000124893

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Differential normal-pulse voltammetry was combined with treated carbon fibre electrodes for monitoring in vivo extracellular catechols synthesized by noradrenergic terminals innervating the paraventricular hypothalamic nucleus. From urethane-anaesthetized rats, pretreated with a monoamine oxidase inhibitor, pargyline, we were able to monitor a catechol signal which unequivocally corresponded to extracellular noradrenaline, and we observed that ether inhalation for 2 min induced an immediate increase in this signal. Electrical stimulation of the ventral noradrenergic pathway (10 Hz for 40 s) induced a similar effect. On the other hand, from freely moving rats which were not treated with pargyline, we recorded a catechol peak which mainly corresponded to 3,4-dihydroxyphenylacetic acid which was synthesized by noradrenergic terminals. However, electrochemical and biochemical evidence strongly suggested that the increase in this signal induced by a 2-min ether stress does not correspond to 3,4-dihydroxyphenylacetic acid, but to an increase in the extracellular noradrenaline concentration. In both experimental situations the time course of the effects was identical: ether stress induced an immediate and pronounced increase in norepinephrine release, and this effect lasted as long as the stimulus duration. This effect appeared specific for noradrenergic terminals, since no effect on dopamine release was observed when recorded from the striatum or behind the paraventricular hypothalamic nucleus from the A13 dopaminergic group. In conclusion, our data are consistent with those which suggest a facilitatory action of norepinephrine on neurose-cretory neurons whose cell bodies are located in the paraventricular hypothalamic nucleus and which play a major role in the hormonal response to stress.

ISSN:0028-3835    

DOI:10.1159/000124894

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Prolactin concentrations were measured in plasma in unanaesthetized male rats chronically prepared with venous and intracerebral cannulae, before and after treatment with bilateral intracerebral injections of serotonin and fenñuramine. Serotonin 1, 5, and 10 nmol injected in the medial basal hypothalamus caused dose-related rises in prolactin concentrations. The secretion of prolactin was blocked by metergoline (2.5 mg/kg i.p.) and only partially by ketanserin (2.0 mg/kg i.v.). The 5-HT 1A agonist 8-OH-DPAT potently stimulated prolactin at doses of 1 and 5 nmol. Fenñuramine 10 and 100 nmol also caused increases in plasma prolactin when injected in the basal hypothalamus. Prolactin secretion was also evoked by serotonin injections in the preoptic/anterior hypothalamic area, but the response was not blocked by serotonin receptor antagonists. It is concluded that activation of 5-HT 1A receptors on or near prolactin-regulating neurons in the arcuate nucleus causes secretion of prolactin. The effectiveness of fenñuramine in increasing plasma prolactin suggests that endogenous serotonin released from terminals in the basal hypothalamus may mediate prolactin secretion physiological

ISSN:0028-3835    

DOI:10.1159/000124895

出版商:S. Karger AG    

年代:1988

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000124896

出版商:S. Karger AG    

年代:1988

数据来源: Karger