摘要:

In fetal and postnatal rats, serum melanophore-stimulating hormone (MSH) levels, pituitary 3H-spiperone binding, pituitary catecholamine content, and other parameters were measured to characterize the development of pars intermedia pituitary control by the tubero-hypophyseal dopamine system. Bioassay of serum for MSH revealed low but significant levels 6 days before birth (gestational day 17), rising to a peak 4 days after birth (postnatal day 5). Levels declined after PN 6, reached a low 2 weeks after birth, and then rose gradually throughout the next several weeks until adult values were attained. From excised pituitaries, significant catecholamine fluorescence in the neurointermediate lobe was first demonstrated on the 2nd postnatal day, with the highest density of fibers being attained at 2 weeks after birth. Thereafter, the density of terminals decreased in the pars intermedia until the adult pattern of innervation was observed at day 60. Total dopamine content of the neurointermediate lobe roughly paralleled the morphological observations through the first 2 weeks after birth. Later, content was seen to stabilize, while concentration decreased in line with the reduction in terminal density. Dopamine levels exceeded norepinephrine concentration by a factor of 10. 3H-spiperone binding sites were present in the pituitary before birth. Their density increased rapidly in the neurointermediate lobe during the first 2 postnatal weeks, then diminished until adult densities were reached at day 30. Binding in the anterior pituitary slowly rose throughout the first 30 days after birth, although values were only about one-quarter of that found in the neurointermediate lobe. In vitro incubation of neurointermediate lobes with dopamine showed a dose-dependent inhibition of spontaneous MSH secretion as early as 2 days after birth. Blockade of dopaminergic binding sites by i.p. administration of cis-flupenthixol (1 mg/kg) to rat pups had no effect until days 8, 15, and 22 where there was a significant rise in serum MSH levels as compared with controls. These data indicate that the intermediate lobe is responsive to dopamine at around birth, while the inhibitory dopaminergic control develops only during the 1st postnatal week, in conjunction with marked changes in circulating MSH levels.

ISSN:0028-3835    

DOI:10.1159/000123947

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

In a previous study we have demonstrated that cervical stimulation (CS) induces α-MSH release. The present experiments were undertaken to (1) examine the pattern of serum α-MSH during CS-induced pseudopregnancy (PSP) and (2) assess the possibility that α-MSH contributes to the induction and maintenance of PSP. Throughout PSP serum α-MSH fluctuated in a cyclic manner demonstrating two daily surges which occurred between 12.00 and 13.00 h (diurnal surge) and between 24.00 and 04.00 h (nocturnal surge). Chronic exposure of animals to α-MSH administered via minipumps (24 µg/day, starting on the morning of estrus), induced PSP as determined by deciduoma formation and persistence of a characteristic diestrous vaginal cytology. Furthermore, insertion of an α-MSH-containing minipump at diestrus 1 (Dl) resulted in progesterone and prolactin (PRL) levels on the afternoon of diestrus 2 (D2) similar to those levels found on day 2 of PSP. Uterine weight was significantly decreased in α-MSH-treated rats and pseudopregnant rats as compared with cyclic D2 controls. α-MSH was found to release PRL indirectly, through stimulation of adrenal progesterone. This effect, however, necessitates the presence of the ovaries as a source of estradiol (EB) since it is demonstrable in intact and acutely ovariectomized rats, but not in chronically ovariectomized animals. EB treatment of chronically ovariectomized rats is capable of restoring the sequence. These results indicate that, as demonstrated for PRL, cervical stimulation initiates rhythmic daily surges of α-MSH secretion which are maintained through PSP. In addition, they suggest that α-MSH may contribute to inducing and maintaining PSP by facilitating the release of adrenal progesterone and by inducing PRL release via the increase in progesterone secretion from t

ISSN:0028-3835    

DOI:10.1159/000123948

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

It has been suggested that in the rat, 5α-androstane-3α, 17β-diol (3α-diol) is physiologically involved in restraining the onset of female puberty. To test this hypothesis several experiments were performed. In normal rats, serum levels of 3α-diol decline slightly during the initial phases of puberty and then sharply several hours before the afternoon preovulatory LH surge on the day of first proestrus. Inhibition of 5α-reductase activity with a highly specific inhibitor, 17β-N, N-diethylcarbamoyl-4-methyl-4-aza-5α-androstane-3-one (4-MA) strikingly depressed both ovarian content and serum levels of 3α-diol, but failed to advance vaginal opening or first ovulation. Administration of different doses of 3α-diol to juvenile rats via Silastic capsules produced a dose-related increase in serum 3α-diol levels. Titers attained ranged from values similar to those of untreated juvenile rats to levels more than 10-fold higher. None of the concentrations, however, inhibited the LH surge and ovulation induced by pregnant mare serum gonadotropin (PMSG). When a similar treatment was administered to normally maturing rats, only the high dose of 3α-diol delayed the age of vaginal opening and of first ovulation. Serum 3α-diol levels attained with this dose were markedly higher than those of untreated juvenile rats (1,086 ± 267 vs. 124 ± 14 pg/ml, respectively). The results indicate that high serum levels of 3α-diol have the capacity to delay the onset of female puberty, but that the prepubertal decrease in serum 3α-diol levels which occurs under normal physiological conditions does not play a significant role in determining the time of puberty. It also appears that juvenile type levels of 3α-diol do not exert a major feedback effect on prepubertal gonadotropin release, and thus they do not represent an important restraining influence on the occu

ISSN:0028-3835    

DOI:10.1159/000123949

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

During the rat estrous cycle, estradiol (E2) and progesterone (P) synergize to activate reproductive behavior. However, receptivity and proceptivity can be elicited by E2 alone in ovariectomized (OVX) animals, particularly when E2 doses are high. The purpose of this study was to determine the neuroendocrine mechanism by which E2 elicits P-dependent reproductive behavior. Adult OVX females received estrogen treatment for 72 h, which consisted of 5 mm Silastic capsules containing 100% E2 or 10% E2, or of 3 injections of estradiol benzoate (EB; 20 µg daily). At 72 h, some animals were sacrificed for nuclear progestin receptor (NPR) measurements, while others were tested for reproductive behavior. The remaining animals received 1 -mg injections of E2, P, moxestrol (Mox) or oil, and either were sacrificed 2 h later for NPR measurements or were tested 4 h later for reproductive behavior. A subset of the animals receiving 1 mg E2 received concurrent administration of the protein synthesis inhibitor, anisomycin (ANI; 100 mg/kg). Acute administration of 1 mg of E2 or P significantly elevated proceptivity, receptivity and NPRs in the mediobasal hypothalamus-preoptic area (MBH-POA) and pituitary (PIT) in females primed with 100% E2. An equivalent dose of Mox was without effect. ANI blocked the acute activation of feminine reproductive behavior by 1 mg of E2. In the absence of acute steroid administration, animals primed for 72 h with EB showed higher levels of reproductive behavior than animals primed with 100% E2 100% E2 10% E2). These results suggest that the actions of E2 via estrogen receptors are not by themselves sufficient to activate feminine reproductive behavior in the rat. The display of high levels of proceptivity and receptivity requires the subsequent activation of neural progestin receptors by P or by E2

ISSN:0028-3835    

DOI:10.1159/000123950

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

In the rat, hypoglycaemia inhibits growth hormone secretion, but the mechanism is unclear. To investigate this further, we have studied the effects of glucose and 2-deoxy-D-glucose on somatostatin and LHRH release from rat hypothalamic fragments incubated in vitro. Glucose (1.35–22 mM) was added to glucose-free medium and 5 and 50 mM 2-deoxy-D-glucose were added to medium containing 5.5 mM glucose. Medium somatostatin and LHRH levels were measured by RIA. Somatostatin and LHRH released diluted in parallel with synthetic somatostatin and LHRH. Sephadex gel filtration demonstrated two molecular forms of somatostatin, 70% coeluting with somatostatin-14 and 30% with somatostatin-28; LHRH coeluted with synthetic LHRH. KC1 (30–100 mM) resulted in release of somatostatin and LHRH; this was reduced in calcium-free medium. Basal and K+-stimulated somatostatin release were significantly increased by reducing glucose levels (r = -0.6, p < 0.001). Basal LHRH was not influenced by glucose. Basal and K+-induced somatostatin release were significantly increased by 2-deoxy-D-glucose (p < 0.05), while LHRH levels remained unchanged. Our results demonstrate that basal and K+-induced somatostatin release from rat hypothalamic fragments are modulated by local glucose concentrations, and this effect is specific as it is not paralleled by LHRH changes. We suggest that the reduction in growth hormone secretion during hypoglycaemia in the rat might be mediated, at least in part, via a direct effect of glucose on somatostatin rele

ISSN:0028-3835    

DOI:10.1159/000123951

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

A method for the enzyme immunoassay (EIA) of delta sleep-inducing peptide (DSIP) has been developed and applied to determine the metabolic clearance rate and biological half-life of DSIP administered to dogs. Antisera to DSIP conjugated to bovine serum albumin were raised in rabbits and proved to be specific for the C-terminus of the peptide. DSIP conjugated to horseradish peroxidase served as the labeled antigen in the EIA and enzyme activity was determined by fluorophotometry. The assay sensitivity was approximately 30 pg/ml. 1 or 2 mg of DSIP was injected intravenously into 4 anesthetized dogs and blood was taken at 5-min intervals. Unextracted plasma was subjected to the EIA directly and showed parallel displacement curves to the standards. DSIP was found to have a rapid disappearance with a mean metabolic clearance rate of 30.7 ± 2.5 ml/kg · min and a mean half-life of 4.0 ± 0.7 min in the dogs. Additional measurements of the metabolic parameters in a monkey and 3 rats treated similarly revealed a rapid in vivo clearance of DSIP from plasma with a half-life of 2.9 and 2.0 ± 0.54 min, respectiv

ISSN:0028-3835    

DOI:10.1159/000123952

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Although LHRH is widely distributed in the diencephalon, previous studies show that testosterone (T) treatment for 72–96 h of castrated male rats raised LHRH levels only in the medial basal hypothalamus. In the present study, LHRH concentrations were analyzed in microdissected brain regions shown to contain LHRH perikarya and their projections to identify the discrete regions which may display this T-dependent accumulation of luteinizing hormone-releasing hormone (LHRH) and to study the temporal sequence of LHRH changes in those regions. Rats were killed at 12-hour intervals from 60 to 96 h after subcutaneous implantation of Silastic® capsules containing T. Results showed that the physiological range of serum T levels attained by these implants suppressed LH release at all times, however, there was no immediate effect on LHRH concentrations in any region. In fact, out of the 9 regions in the preoptic-tuberal pathway examined, 8 regions displayed no change in LHRH concentrations at any time. On the other hand, for up to 84 h, LHRH concentrations in the median eminence region remained unchanged; an additional 12 h of T exposure significantly raised LHRH levels. These results suggest that this T-dependent accumulation of LHRH may arise either by de novo synthesis or by increase in the rate of processing of the precursor LHRH protein into the immunoreactive form within nerve terminals in the median eminen

ISSN:0028-3835    

DOI:10.1159/000123953

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Synthetic ovine corticotropin releasing factor (CRF) at 0.03–30 ng/ml evoked a significant linear release of ACTH in pituitary monolayer cell cultures. Arginine vasopressin (AVP) at 3–30 ng/ml induced a slight ACTH release in the same culture system. CRF at 100 ng/ml greatly increased the medium ACTH with intracellular ACTH remaining relatively constant. In perifused pituitary quarters, both AVP and CRF evoked significant release of ACTH. When AVP was added in combination with synthetic ovine CRF, an additive or synergistic effect was observed on the CRF-induced ACTH release in both in vitro systems. Preincubation of cultured pituitary cells with synthetic ovine CRF for 1 h did not have a significant effect on the subsequent AVP-induced ACTH release. However, when cells were preincubated for 6 h with CRF at 1 and 100 ng/ml, the AVP-induced ACTH release was significantly increased, but preincubation with AVP suppressed both the basal and AVP-induced ACTH release. These results suggest that synthetic ovine CRF stimulates not only the release of ACTH but also the synthesis of ACTH and that AVP can evoke significant ACTH release from corticotrophs which have enough releasable ACTH or substances needed for ACTH release under the influence of

ISSN:0028-3835    

DOI:10.1159/000123954

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Recent evidence demonstrating a direct effect of 5-hydroxytryptamine (5-HT) upon anterior pituitary (AP) hormone secretion has made the question of determining the location of possible sites that could supply 5-HT to the AP an important one. It has been assumed, based on indirect evidence, that aromatic L-amino acid decarboxylase (L-AAD), the enzyme responsible for the conversion of L-5-hydroxytryptophan (5-HTP) to 5-HT as well as L-3,4-dihydroxyphenylalanine (L-dopa) to dopamine (DA), is ubiquitously distributed in most tissues of the body including the AP. The present study examined the ability of the AP and two neural areas anatomically connected to the AP, the neurointermediate lobe () of the pituitary and the median eminence (ME), to decarboxylate 5-HTP to 5-HT or L-dopa to DA following either the in vitro incubation of the various tissues with 5-HTP or L-dopa or the in vivo administration of 5-HTP to rats treated previously with saline or a peripheral decarboxylase inhibitor, MK486. The in vivo effects of 5-HTP, alone, or following MK486 pretreatment were also examined on 5-HT synthesis and metabolism in AP tissues which were transplanted 5 days previously under the renal capsule and were, thus, isolated from central influences that might be regulating 5-HT and 5-hydroxyindole-3-acetic acid (5-HIAA) concentrations in the animal’s own AP. In addition, the direct radioisotopic measurement of L-AAD activity in the ME, , and AP was also analyzed. The data demonstrate that, unlike the ME or , the AP lacks the capacity to decarboxylate 5-HTP to 5-HT or L-dopa to DA and is therefore dependent on other sources to account for its 5-HT, 5-HIAA, and DA content. Furthermore, the results implicate a central source(s) in supplying a large portion of the 5-HIAA found in the animal’s own AP, and suggest that although the contribution of centrally synthesized 5-HT to basal AP 5-HT concentrations may not be a major one, under circumstances where central L-AAD-containing areas are greatly stimulated, the newly synthesized 5-HT can affect 5-HT concentrations in the

ISSN:0028-3835    

DOI:10.1159/000123955

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

To evaluate whether ovarian steroid environment may modify endogenous opioid activity at hypothalamic-pituitary level, the effects of naloxone infusion (1.2 mg/h for 4 h) on gonadotropin secretion were studied in 5 postmenopausal women who had natural menopause 3–5 years before the study. In addition, naloxone infusion was repeated in the same subjects after chronic oral treatment with conjugated estrogens (1.25 mg/day in two divided doses for 20 days). Before treatment, both the circulating levels of estrogens and plasma gonadotropins were in the normal range for postmenopausal women and naloxone infusion did not induce any significant modification of gonadotropin secretion. In contrast, after estrogen therapy, and the consequent rise in estrogen plasma levels, naloxone infusion induced a significant LH increase (p < 0.01) starting during the last hour of treatment. These findings seem to confirm that endogenous opioid peptides may modulate the inhibitory effect exerted by estrogens on LH secretion, in human

ISSN:0028-3835    

DOI:10.1159/000123956

出版商:S. Karger AG    

年代:1984

数据来源: Karger