摘要:

The effects of synthetic enkephalin analog (FK 33–824) and β-endorphin on growth hormone (GH) secretion and their interaction with brain monoamines were investigated in unanesthetized male rats. Blood samples (0.4 ml each) were withdrawn every 10–20 min for 6 h from a catheter chronically implanted in the right atrium. In all control rats, immunoreactive GH secretion was pulsatile in nature and two major GH bursts were found to occur around 12.00 and 15.30.The opioid peptides were injected between bursts at 14.00. Following an intravenous administration of FK 33–824 (10 μg/100 g b.w.), there was an abrupt increase in plasma GH, which was significantly suppressed by naloxone (125 μg/ 100 g b.w., i.v.), a specific opiate antagonist. Pretreatment with reserpine (1 mg/100 g b.w., i.p.) abolished not only the natural GH burst but also the GH response to FK 33–824. Pretreatment with dopamine-β-hydroxylase inhibitors, diethyldithiocarbamate (DDC, 100 mg/100 g b.w., i.v.) and fusarate (10 mg/100 g b.w., i.v.) also inhibited the natural GH burst and GH rise induced by FK 33–824. Intravenous injection of clonidine (15 μg/100 g b.w.), an α-adrenergic stimulant, resulted in an increase in plasma GH in the rats pretreated with reserpine, DDC or fusarate. Phenoxybenzamine (1 mg/100g b.w., i.v.), an α-adrenergic blocking agent, inhibited the GH response to FK 33–824. On the other hand, GH release induced by FK 33–824 was not influenced by propranolol (1 mg/100 g b.w., i.v.), a β-adrenergic blocking agent, nor pimozide (0.1 mg/100g b.w., i.v.), a dopamine antagonist. Intraventricular administration of β-endorphin (5 μg/rat) also increased the plasma GH levels which were lowered by phenoxybenzamine. These findings suggest that α-adrenergic mechanisms are involved in GH release induced by op

ISSN:0028-3835    

DOI:10.1159/000123216

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

Peristalsis in the guinea pig isolated ileum usually consists of alternating periods of activity and peristalsis-free intervals (PFIs). When PFIs were shorter than, on an average, 5 min, somatostatin at 10–9 or 10–8M prolonged subsequent PFIs. By contrast, when PFIs were longer than 5 min, somatostatin shortened subsequent PFIs. No evidence could be found for an interaction of somatostatin with opioid mechanisms. The present work demonstrates that the action of a substance upon intestinal peristalsis in vitro may depend, at least in the case of somatostatin, upon the functional state of the isolated intestinal segm

ISSN:0028-3835    

DOI:10.1159/000123217

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

A specific opiate antagonist, naloxone, administered i.v. to 5 normal men at the doses of 0.4 mg or 0.8 mg in bolus, did not modify basal PRL, GH, TSH and FSH levels, but significantly increased basal LH concentrations at the dose of 0.8 mg. Naloxone at both doses was also able to significantly enhance the response of TSH to a TRH stimulation test (TRH 400 μg i.v. in bolus) but did not alter significantly the PRL response. These results suggest that endogenous opioid peptides may have an influence on the modulation of LH secretion in basal conditions and on the responsiveness of TSH to dynamic stimulation by TRH

ISSN:0028-3835    

DOI:10.1159/000123218

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

The effects of aging on the responsiveness of the neuroendocrine system to ovariectomy and estrogen replacement were determined. Neuroendocrine responsiveness in young (6-month-old) cyclic rats was compared to that in old (24-month-old) constant estrous rats. Seven neuroendocrine parameters were examined: median eminence (ME) concentrations of norepinephrine (NE), dopamine (DA) and luteinizing hormone-releasing factor (LRF) and circulating concentrations of LH, FSH, prolactin (PRL) and 17β-estradiol (E2). These concentrations were measured in intact and ovariectomized rats and in ovariectomized rats treated for 3 weeks with E2. 3 weeks after ovariectomy of young rats the ME concentrations of NE (38.0 ± 10.4 pg/μg, n = 15) and DA (201 ± 32 pg/μg, n = 15) were significantly higher (p < 0.05) than the respective levels in intact proestrous controls (18.7 ± 1.9 pg/μg, n = 18) and 89.4 ± 12.4 pg/μg, n = 18). In old rats there was no significant change in ME concentration of NE after ovariectomy. ME DA levels in old rats did rise after castration by 62%; however, this rise was only half of that in young animals (125%). The increases in DA after ovariectomy could be completely reversed by E2 in both young and old rats. ME concentration of LRF was reduced after castration to a similar extent in young (76%) and old (81 %) rats, and these effects were partially E2-reversible in both age groups. The postovariectomy increases in LH (485%) and FSH (665%) in young rats were greater than the respective increases in old rats (169 and 191%). In contrast, the changes in PRL concentration following ovariectomy and E2 replacement were similar in magnitude in both age groups. The present results indicate that the neuroendocrine responsiveness to ovariectomy is altered during aging. This alteration in responsiveness is selective, in that changes were demonstrable in only 2 out of 7 parameters

ISSN:0028-3835    

DOI:10.1159/000123219

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

The corticostimulating activity of the fetal rat hypophysis was studied on day 21, in fetuses deprived of their hypothalami by total removal of the brain (encephalectomy) in early (day 16) or late (day 19) stages of gestation. On day 19, the fetal manipulation was performed either on intact or adrenalectomized dams. The data show that: (1) Compared to controls, encephalectomy does not alter pituitary ACTH content in fetuses of intact mothers but that pituitary ACTH content does not significantly increase in encephalectomized fetuses of adrenalectomized mothers whereas it does in the littermate control fetuses. (2) Compared to controls, circulating ACTH levels are reduced by encephalectomy on both day 16 and day 19; an increase in ACTH levels occurs in both fetal groups in response to maternal adrenalectomy. Decapitation removes this fetal source of ACTH. (3) Adrenal glands are not as much atrophied by encephalectomy as by decapitation on day 16, whereas adrenal weight is decreased to the same extent by encephalectomy and by decapitation on day 19. However, the marked increase in circulating ACTH in both control and encephalectomized fetuses caused by maternal adrenalectomy is probably the cause of the significant increase in adrenal weight in these groups. (4) Adrenal corticosterone content in all the groups but not always adrenal weight, is a fairly accurate reflection of the ACTH levels measured. The results suggest that: (1) Pituitary ACTH content is not a sensitive measure of dynamic changes in synthesis and secretion in rat fetuses. (2) Changes in basal plasma ACTH in response to fetal encephalectomy show the presence of both an autonomous corticotropic function and a cephalic regulation of the corticotropic function from day 16 of fetal life and beyond. Pituitary autonomy seems higher in earlier than in later stages of gestation. (3) There is feedback of corticosterone into the pituitary of fetal rats; a marked increase in ACTH release is caused by the removal of the maternal corticosteroids.

ISSN:0028-3835    

DOI:10.1159/000123220

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

Intracisternal (i. c.) administration (25 μg or 42.6 nmol) of the potent met-enkephalin analog, D-ala2-met-enkephalinamide (DALA) in adult male rats increased plasma concentrations of norepinephrine and epinephrine for more than 90 min. Intra-arterial (i.a.) administration of the same or a fourfold larger dose was without any effect. I.e. administration of human β-endorphin (25 μg or 7.25 nmol) produced much greater plasma responses of all three catecholamines than seen with DALA. An i.a. dose of naloxone, which had been shown previously to inhibit the plasma catecholamine responses to β-endorphin, failed to inhibit plasma catecholamine responses to DALA. Also, naloxone alone failed to alter the basal plasma concentrations of the three catecholamines. The data are consistent with an effect of DALA acting at a presently unknown brain site to increase central sympathetic outflow, thus increasing plasma concentrations of norepinephrine and epinephrine. It appears probable that this effect of DALA is mediated at a different opioid receptor and perhaps a different brain site than the effect of β-endorphin to increase central sympathetic out

ISSN:0028-3835    

DOI:10.1159/000123221

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

Cell nuclear estrogen receptors and cytosol progestin receptors were measured in the pituitary gland, preoptic area and hypothalamus throughout the estrous cycle of the rat. Cell nuclear estrogen receptor levels paralleled changes in serum estradiol cencentrations with highest values on proestrus and lowest on diestrus. Proestrous values were 50–60% of capacity for each tissue. Cytosol progestin receptor number in these tissues was also highest on proestrus and lowest on diestrus. With these data as a guide, Silastic capsules filled with estradiol-cholesterol mixtures were used to generate physiologic levels of estrogen receptor occupation within the brain-pituitary complex of ovariectomized rats and to examine the kinetics of estradiol stimulation of lordosis behavior and cyclic gonadotropin release. Our results indicate that the effectiveness of an estradiol stimulus to elicit lordosis or luteinizing hormone release depends on at least three factors: the magnitude of the increment in serum estradiol and brain and pituitary cell nuclear estradiol receptor levels; the duration over which these increments are maintained; and the interval from previous exposure to estroge

ISSN:0028-3835    

DOI:10.1159/000123222

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

Wistar female rats were treated with 1.25 mg testosterone propionate (TP) on day 5 (day of birth = day 1). The hypothalamic arcuate nucleus (ARCN) in the brains of normal and neonatally TP-treated (androgenized) females was examined ultrastructurally at 6, 10, 20, 45 and 100 days of age. Axodendritic shaft and spine synapses were counted in a field of 10,000 μm2 of the neuropil in the middle part of the ARCN in each brain. The mean numbers of shaft and spine synapses both in normal and androgenized females increased from days 6 to 45, and reached a plateau by day 45. The mean number of shaft synapses in androgenized females was not significantly different from that in normal controls at each age. No significant difference in the number of spine synapses between normal and androgenized rats was seen 1 day after TP administration (sacrificed at 6 days of age). However, the incidence of spine synapses in androgenized females 5 days after TP injection (sacrificed at 10 days of age) was significantly smaller than that in the controls. This tendency became much clearer during the course of postnatal development. Since the synaptic organization of the ARCN in normal adult males is quite homologous to that observed in the androgenized adult females in the present study, it is suggested that androgen given neonatally is responsible for sexual differentiation of the synaptic pattern in the ARCN and that this synaptic difference develops from the early postnatal period

ISSN:0028-3835    

DOI:10.1159/000123223

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

The effects of intraventricular (i.v.t.) morphine sulfate (MS) and β-endorphin (β-EP) on pituitary-adrenal activity and the release of pituitary β-EP were studied in rats. Pituitary-adrenal activity was monitored by measuring plasma corticosterone (CS) levels. 45 min after i.v.t. injection, both MS and β-EP caused dose-related increases in plasma CS, with β-EP being approximately ten times more potent on a molar basis. MS injected i.v.t. at 0.3, 1.0, 3.0 and 10.0 μg did not cause a significant reduction in pituitary immunoreactive (i.r.) β-EP, but did cause an increase in plasma i.r. β-EP at 3 μg of MS. β-EP injected i.v.t. at 1.5 μg caused a reduction of pituitary i.r. β-EP. Since i.v.t.-injected β-EP may have contributed to the measured plasma i.r. β-EP, a nonimmunoreactive analog (Des-Asn20-βc-EP) was used to assess the change in plasma i.r. β-EP. 5 μg of Des-Asn20-βc-EP injected i.v.t. caused increases in plasma i.r. β-EP and CS, as well as a 40% reduction in pituitary i.r. β-EP. The concomitant intraperitoneal (i.p.) injection of naloxone HC1 (10 mg/kg) significantly blocked the increase in plasma CS induced by 5 μg of β-EP. When naloxone HC1, 10 mg/kg was injected alone, a significant increase in plasma CS was found. The results indicate that i.v.t. β-EP is more potent than MS in causing the release of pituitary ACTH and β-EP. These findings are consistent with a role for brain endorphins in the re

ISSN:0028-3835    

DOI:10.1159/000123224

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

We have investigated the effects of exposure to short-term constant light (LL) on the spontaneous, proestrous luteinizing hormone (LH) surge in the female rat. Exposure to LL during the 3 days preceding proestrus delayed and reduced the magnitude of the LH surge which was measured in blood samples taken from conscious animals through an intra-atrial catheter that had been implanted early on the morning of proestrus. The pituitary responsiveness to synthetic luteinizing hormone-releasing hormone (LHRH) in animals exposed to LL was reduced about 6-fold about the time of the LH surge compared with that in animals on a 14 h light-10 h dark (LD) regimen. In contrast to animals on LD, treatment of rats on LL with estrogen and progesterone after ovariectomy failed to restore to normal the pituitary responsiveness which is markedly reduced by ovariectomy. The implantation of a silicone-elastomer capsule containing 17β-estradiol into rats on LL after ovariectomy did not facilitate pituitary responsiveness. These results suggest that exposure of the female rats to LL for 3 days causes a shift in phase of the LH surge (which may represent a free-running LH rhythm) and reduces the magnitude of the LH surge by a mechanism which may involve a reduction in the sensitivity to estrogen of the centres involved in LHRH release

ISSN:0028-3835    

DOI:10.1159/000123225

出版商:S. Karger AG    

年代:1981

数据来源: Karger