摘要:

Accumulations of 5-hydroxytryptophan (5HTP) and L-dihydroxyphenylalanine (L-DOPA) following decarboxylase inhibition as indices for 5-hydroxytryptamine (5HT) and catecholamine (dopamine and/or norepinephrine) synthesis, respectively, were both increased in the preoptic area-anterior hypothalamus (POA-AH) of ovariectomized rats treated with a combination of 17β-estradiol benzoate (E2) and progesterone (P). Similarly, an increased accumulation of L-DOPA was seen in the mediobasal hypothalamus (MBH) and median eminence (ME) of these animals although no change was observed in 5HTP accumulation in the MBH or ME of these rats. Hypophysectomy negated these steroid-induced effects on L-DOPA accumulation. However, hypophysectomy had no apparent effect on steroid-stimulated 5HTP accumulation in the POA-AH of these rats. Under the experimental conditions of our study, the results suggest (1) that the stimulatory effect of ovarian steroids on hypothalamic catecholamine synthesis is dependent on an intact pituitary gland, (2) that the stimulatory effect of ovarian steroids on 5HT synthesis in the POA-AH is not dependent on an intact pituitary gland, and (3) that ovarian steroids do not seem to influence 5HT synthesis in the ME or MBH. The significance of these results may lie in the function of these hypothalamic monoaminergic neurotransmitter systems to regulate gonadotrophin release and subsequent steroid feedback modulation of such central regulatory mechanisms

ISSN:0028-3835    

DOI:10.1159/000124461

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Female Ames dwarf and phenotypically normal female mice were killed 30 min after treatment with NSD-1015, an aromatic L-amino acid decarboxylase inhibitor. The accumulation of dihydroxyphenylalanine (DOPA) and 5-hy-droxytryptophan were measured by high-performance liquid chromatography with electrochemical detection and provided estimates of the endogenous biosynthesis of dopamine (DA) in the median eminence (ME) and serotonin biosynthesis (5-HT) in all brain regions which were examined. Dopamine synthesis was markedly suppressed in the ME while 5-HT synthesis was enhanced in both the ME and mediobasal hypothalamus (MBH) of dwarfs as compared to phenotypically normal mice. Overall, catecholamine biosynthesis (DOPA accumulation) was suppressed in the MBH of the dwarf mice but was not different from that observed in normal mice in the preoptic area anterior hypothalamus (POA-AH). The biosynthesis of 5-HT was not different in the POA-AH of dwarf mice as compared to normal mice. In the second experiment dwarf mice received saline vehicle, ovine prolactin (PRL), growth hormone (GH) or thyroxin (T4) daily for 14 days. Normal mice received saline only. Replacement with PRL significantly enhanced DA synthesis in the ME and was the only hormone to suppress significantly the elevation of 5-HT synthesis normally observed in the ME and the MBH of the dwarfs. Both GH and T4 only partially reduced 5-HT synthesis in the ME and MBH so that this parameter was no longer statistically different from either saline-treated dwarfs or normal mice. These results suggest that the deficiency of DA in the dwarf mouse ME may be due in part to a reduced synthesis of this amine in the tuberoinfundibular dopaminergic neurons, and PRL replacement is most effective in elevating this parameter to a level approaching that observed in normal mice. The enhancement of 5-HT synthesis in the ME and MBH of the dwarfs may reflect the absence of a normal inhibitory feedback effect of circulating PRL on this parameter. Such a mechanism would be suggestive of a potential stimulatory role for hypothalamic 5-HT in regulating PRL secretion. Potential relationships between hypothalamic 5-HT and GH or T4 are less clearly demonstrable but cannot be discounted.

ISSN:0028-3835    

DOI:10.1159/000124462

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Both the pituitary-adrenal axis and the pituitary-gonadal axis are under the tonic inhibitory control of endogenous opioid peptides in man. However, the precise opioid receptor involved in the modulation of these hormones remains unknown. The effect of a dose of intravenous naloxone on serum levels of luteinising hormone (LH), follicle-stimulating hormone (FSH) and plasma cortisol was therefore investigated in ten normal subjects. In the male subjects, naloxone at a dose of 25 µg/kg caused a significant increase in serum LH and FSH; no increase in response was seen at the two higher doses (100 µg/kg and 250 µg/kg). The lowest dose (6 µg/kg) caused no change in serum LH and FSH. In the female subjects, tested in the early follicular phase of their cycles, no dose of naloxone significantly increased circulating gonadotrophins. In both male and female subjects, naloxone only stimulated a rise in serum cortisol at the highest dose (250 µg/kg). A second study in six normal subjects demonstrated that the rise in cortisol with the highest dose of naloxone was secondary to a rise in plasma ACTH. It is concluded that the opioid receptor(s) controlling gonadotrophin release in man are naloxone-sensitive, and are probably epsilon-receptors; the naloxone insensitivity of the pituitary-adrenal axis suggests that these responses are modulated by kappa- or delta-recep

ISSN:0028-3835    

DOI:10.1159/000124463

出版商:S. Karger AG    

年代:1986

数据来源: Karger