摘要:

The capacity of various pregnanes for counteracting androgen-induced defeminization was evaluated in an attempt to define some cellular mechanisms involved in the defeminization process. 5-day-old female rats received 60 µg testosterone propionate (TP) along with one of various pregnanes:progesterone, 5β-pregnandione, 5β,3α-pregnanolone, 5β,3β-pregnanolone, 5α-pregnandione, 5α,3β-pregnanolone, 5α,3α-pregnanolone or chlormadinone acetate. Protection against defeminization was defined as a significantly smaller proportion of anovulatory animals in a group compared to the control TP group. Data were analyzed at 60, 90 and 120 days of age. The anesthetic potency of the pregnanes was evaluated in 5-day-old male rats through the analysis of EEG and EMG records. Anesthetic pregnanes – progesterone, 5β-pregnandione and 5β,3α-pregnanolone – counteracted defeminization while nonanesthetic pregnanes – 5α-pregnanes, chlormadinone acetate and 5β,3β-pregnanolone – did not. The results show a clear relation between anesthetic capacity and protectio

ISSN:0028-3835    

DOI:10.1159/000123328

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

The 24-hour rhythm of retinal and hypothalamic melatonin immunofluorescence was determined in male albino rats and compared to the 24-hour rhythm of serum melatonin determined by radioimmunoassay. Under a 12-hour (0:00–12:00):12-hour dark cycle, the 24-hour rhythm of melatonin immunocytochemical fluorescence in the retina was bio-modal (crests at 1:00 and 10:00–13:00). In serum, melatonin has a single crest late in the dark period (18:00). In the hypothalamus melatonin immunofluorescence showed increments corresponding to the crests in retina (13:00) and serum (18:00). In a 2-hour light: 22-hour dark cycle, the retinal rhythm was suppressed, the serum rhythm unchanged, and the hypothalamic rhythm had a single crest corresponding to the crest of the serum melatonin rhythm. These data indicate that the 24-hour hypothalamic rhythm of melatonin immunofluorescence may be secondary to the serum and retinal 24-hour rhythms of melato

ISSN:0028-3835    

DOI:10.1159/000123329

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

Administration of benzodiazepines to male or female rats was observed to inhibit prolactin release. Basal secretion of prolactin was only slightly suppressed with the highest dose of benzodiazepines; however, the rise in prolactin release following a stimulus was prevented even at low doses (0.1–1 mg/kg). The benzodiazepine diazepam blocked stress-induced prolactin release and, when given during the critical period of proestrus, the proestrus surge of prolactin. Diazepam administration also blunted the release of prolactin induced by dopaminergic receptor blockade following haloperidol, or by serotonergic receptor activation produced by fluoxetine, a serotonergic reuptake inhibitor plus 5-hydroxytryptophan, a serotonin precursor. Inhibition of prolactin release by benzodiazepine was dose related, and inhibition was still evident after repeated diazepam injection. The potency of three benzodiazepine analogues to inhibit prolactin release correlated with their potency to displace radiolabeled diazepam binding from brain membrane fractions or to induce other biological responses (clonazepam > diazepam > chlordiazepoxide). These actions of benzodiazepines on prolactin release are similar to those reported for γ-aminobutyric acid (GABA). The hypothesis of a benzodiazepine GABA receptor complex suggests that GABA may be involved in these in vivo actions of diazep

ISSN:0028-3835    

DOI:10.1159/000123330

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

The effect of hypophysectomy on the number of corticosterone receptor sites was investigated in three rat brain regions and was compared with the effect of long-term adrenalectomy. Subsequently, the effect on receptor capacity was measured after the hypophysectomized rats had received as substitution therapy ACTH1-24 and smaller peptide fragments lacking corticotropic activity. All rats (sham and hypophysectomy) were adrenalectomized 24 h prior to sacrifice for depletion of endogenous adrenal hormones and replacement therapy was discontinued at that time. Extensive perfusion with saline was carried out at the time of sacrifice. 3H-corticosterone binding was measured in cytosol by means of an in vitro assay. 2 weeks after hypophysectomy, the apparent maximal binding capacity (Bmax) of the corticosterone receptor system was increased by 60, 36 and 72% in hippocampus, hypothalamus and septum, respectively. The increase in Bmax in the hippocampus of hypophysectomized rats was 30% higher than the increase in animals adrenalectomized 2 weeks previously. Replacement with ACTH1-24 markedly decreased the binding capacity in all brain regions investigated. Replacement with the behaviorally active ACTH4-10 sequence reduced the number of corticosterone receptor sites in the hippocampus by 21%, while the behaviorally inactive ACTH11-24 sequence was ineffective. Des-glycinamide-arginine-vasopressin was also ineffective. There were no alterations in binding affinity for corticosterone in hippocampal cytosol after the surgical procedures or after the different replacement therapies. It is concluded that the neurotropic ACTH4-10 sequence reduces the number of corticosterone receptor sites in the hippocampus of the hypophysectomized rat. The action of ACTH4-10 was specific for the hippocampus and was not observed in other brain regions or plasma transcortin.

ISSN:0028-3835    

DOI:10.1159/000123331

出版商:S. Karger AG    

年代:1982

数据来源: Karger