摘要:

Cytosol from the spinal cord (SC) of adrenalectomized rats was incubated with a range of [3H]-aldosterone (ALDO) concentrations and the results analyzed according to Scatchard. High affinity (Kd < 1 nM) as well as low affinity (Kd 30–195 nM) sites were measured; the low affinity site was abolished by co-incubation with the pure antiglucocorticoid RU 28362. [3H]-ALDO in concentrations shown to bind to the high affinity site only, was completely displaced by the spirolactone, RU 26752, but not by RU 28362; however, the latter compound competed for 40% of the sites when incubated with a higher (10 nM) concentration of [3H]-ALDO, binding approximately one-half to each receptor type. The high affinity site was distributed uniformly in four sections of the SC, with significantly lower levels in the region corresponding to the filum terminale and horse tail and slightly higher in the cervical and lumbar enlargements. The high affinity site acquired increased affinity for DNA-cellulose after heat-induced transformation, with reduced capacity to bind to DEAE-cellulose. These results suggest that the SC contains, in addition to glucocorticoid receptors, binding molecules of high affinity and stereoselectivity for mineralocorticoids, and that, under appropriate conditions, present increased affinity for DNA acceptor site

ISSN:0028-3835    

DOI:10.1159/000124556

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

The effects of somatostatin and dopaminergic agents on pituitary cyclic nucleotide phosphodiesterases that had been partially purified through DEAE cellulose column chromatography were studied. Somatostatin, .L-dopa, dopamine and CB-154(2-bromo-α-ergocriptine) competitively inhibited the pituitary cyclic AMP phosphodiesterase activity, especially that of the low Km enzyme. This inhibition was most potent in the case of somatostatin and CB-154

ISSN:0028-3835    

DOI:10.1159/000124557

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

The preoptic area (POA) of the male ring dove is a target for specific behavioral effects of estrogen that are separable from those of androgen. Activity of the aromatase system in the POA, which converts testosterone to 17β-estradiol (E2 1.0 mm from POA nuclei were ineffective in increasing preoptic aromatase activity irrespective of whether the implants were unilateral, or bilateral with twice the potential output of testosterone. Within the 1.0-mm range, distance of implant from the POA nuclei was negatively correlated with induced aromatase activity in POA samples, indicating a direct effect of testosterone or its metabolites on enzyme activity. Induction of aromatase activity was higher in the right side of the POA than the left, suggesting asymmetry in inducible aromatase. Inactive 5β-reduced androstanes, 5α-dihydrotestosterone and 17β-estradiol were formed from intracranial 3H-testosterone in POA. Since estradiol benzoate implants did not induce aromatase activity, this metabolite does not appear to act directly on the POA, although it is effective if administered systemically. Implants of TP in the region of the POA caused vocal behavior (perch calling) to be shown by some males. There was no correlation between the behavioral effectiveness of implants and induced POA aromatase activity. Since increase in E2 formation occurred in the absence of vocal behavior, activation of androgen-dependent behavior is not an absolute requirement for the induction effect. We conclude that testosterone can influence aromatase activity required for local production of E2 in the brain by direct action on POA ce

ISSN:0028-3835    

DOI:10.1159/000124558

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

The aim of the present study was to evaluate whether arachidonic acid metabolism may play a role on luteinizing hormone (LH) and prolactin (PRL) release directly at the pituitary level. To this purpose, exogenous arachidonic acid, alone or in presence of inhibitors of cycloxygenase (indomethacin:IND) and lipoxygenase pathways (nordihydroguaiaretic acid:NDGA), was added to perfused rat anterior pituitary cells. PGE, PGFα, LH and PRL levels present in the eluate were assayed with specific RIA methods. Both PGE and PGFα show a dose-related response after the addition of increasing doses of arachidonic acid. The addition of 0.05 mM arachidonic acid induces an increase of LH and PRL. The addition of IND to the perfusion medium highly potentiates the stimulatory effects induced by arachidonic acid on LH and PRL release. On the contrary, the addition to the medium of either NDGA or IND plus NDGA completely reverses the stimulatory action induced by arachidonic acid alone. The present results suggest that: (1) adenohypophyseal cells are able to metabolize exogenous arachidonic acid; (2) arachidonic acid induces an elevation in LH and PRL levels; (3) lipoxygenase pathway metabolite(s) are likely involved in these activities, and (4) the site of action of arachidonic acid is at the pituitary leve

ISSN:0028-3835    

DOI:10.1159/000124559

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

The aim of this study was to investigate the involvement of somatostatin (SRIF) in the thyrotroph adaptation to nutritional changes. For this purpose, we studied the effects of passive immunization with SRIF antiserum (A-SRIF) on the reduced basal TSH secretion in rats starved for 72 h and on the plasma TSH surge following carbohydrate (CHO) refeeding. This latter experiment was performed at two different times of the day in order to elucidate whether SRIF may participate in the regulation of the plasma TSH circadian rhythm. In chronically catheterized rats, we observed that A-SRIF injection induced a similar pattern of plasma TSH rise over a sampling period of 5½ h in both fed and rats starved for 72 h (3-way analysis of variance). In morning experiments, CHO refeeding or A-SRIF injection elicited a significant rise in plasma TSH. The amplitude and duration of the response was proportional to the injected dose. In evening experiments, although basal TSH values were significantly lower than those observed in the morning ones, maximal plasma TSH values after A-SRIF injection were not significantly different. At both times of the day, association of refeeding and A-SRIF injection did not stimulate TSH further than either refeeding alone or A-SRIF alone. In conclusion, our data suggest that SRIF (1) cannot account for the differences in serum TSH levels between fed and starved rats; (2) is not responsible for the diurnal difference in basal serum TSH in starved rats, and (3) seems to be involved in the TSH response to refeeding

ISSN:0028-3835    

DOI:10.1159/000124560

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Excessive exposure to glucocorticoids can damage neurons of the hippocampus, the principal neural target tissue for the steroid. Glucocorticoids, which are broadly catabolic throughout the body, appear to damage the hippocampus by inducing a metabolic vulnerability in its neurons, impairing their capacity to survive varied neuropathologic challenges which would normally be sublethal. As such, a number of interventions which damage the hippocampus – infusion of an excitotoxin or of an antimetabolite or induction of global ischemia – have their toxicity enhanced in rats with high circulating corticosterone concentrations and attenuated in adrenalectomized animals. The present report examines the temporal parameters with which corticosterone modulates the toxicity of the excitotoxin kainic acid (KA). Rats adrenalectomized and maintained corticosterone-free for 1 week prior to and following microinfusion of KA had minimal volumes of hippocampal damage. Administration of 10 mg/day of corticosterone (which produces circulating concentrations in the upper physiological range for the majority of a day) for as little as 1 day prior to and following KA infusion significantly potentiated damage; increasing periods of exposure to corticosterone bracketing the infusion of the toxin progressively increased damage. Both exposure to corticosterone only during the period prior to KA infusion or only in the aftermath of infusion potentiated damage. Thus, glucocorticoids appear to compromise the capacity of hippocampal neurons to survive KA via both rapid effects (manifest within as little as 24 h) as well as through more persistent acti

ISSN:0028-3835    

DOI:10.1159/000124561

出版商:S. Karger AG    

年代:1986

数据来源: Karger