摘要:

In a previous study, we demonstrated that progesterone (P4) and the synthetic glucocorticoid triamcinolone acetonide (TA), but not cortisol, could induce LH and FSH release in estrogen-primed ovariectomized immature rats. Therefore, the purpose of this study was to determine if the stimulatory effect of P4 and TA on LH and FSH release were associated with changes in GnRH or NPY concentrations in the medial basal hypothalamus (MBH) or preoptic area (POA). Ovariectomized immature rats primed with estradiol at 27 and 28 days received either vehicle, P4, TA or cortisol (1 mg/kg BW) at 9.00 h on day 29. Animals were killed at 9.30, 10.00, 12.00 and 13.00 h on day 29 for serum LH and FSH measurements, and the MBH and POA were dissected and analyzed for GnRH and NPY concentrations via RIAs. P4- and TA-treated animals showed significantly elevated serum LH and FSH levels from 13.00 h to 15.00 h. Cortisol was without effect. P4 significantly increased MBH GnRH and NPY concentrations at 12.00 h followed by a significant fall at 13.00 h. P4 modulated POA GnRH and NPY concentrations in a fashion similar to that seen in the MBH, except POA NPY concentrations did not fall at 13.00 h after the elevation at 12.00 h. TA had no significant effect on MBH GnRH and NPYlevels at 12.00 h compared to the values at 9.30 h and 10.00 h but, as with P4, there was a significant fall in MBH GnRH and NPY levels at 13.00 h. TA had no significant effect on POA GnRH and NPY concentrations at any time point studied. Consistent with its lack of effect on serum LH and FSH, cortisol had no effect on MBH GnRH and NPY. Interestingly, cortisol significantly increased POA LHRH and NPY at 12.00 h followed by a fall at 13.00 h. However, cortisol had no effect on LH and FSH levels on the day of administration. In summary, the stimulatory effects of P4 and TA on LH and FSH release in the estrogen-primed ovariectomized immature rat appear to be mediated by a similar mechanism involving changes in MBH and POA GnRH and NPY concentrations.

ISSN:0028-3835    

DOI:10.1159/000125930

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

Bilateral electrolytic lesions of the incertohypothalamic A13 dopamine (DA) system were made on the morning of proestrus in female rats with regular estrous cycles under ether anesthesia. Hourly blood samples were withdrawn, via a jugular catheter from conscious, freely moving rats, between 14.00 h and 18.00 h on the afternoon of proestrus. Plasma LH, FSH and prolactin levels were determined by RIA. The preovulatory surges of LH and prolactin were blocked in animals in which the A13 DA nucleus was destroyed by more than 70%. Levels of FSH were not significantly different from those of control or sham-lesioned groups. Lesions that were dorsal, ventral or caudal to the A13 DA systems did not affect the preovulatory surges of LH and prolactin whereas anterior lesions caused variable changes in the level of all three hormones. These data suggest that the A13 DA region may have a role in the control of the preovulatory surges of LH and prolactin.

ISSN:0028-3835    

DOI:10.1159/000125931

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

Chronic administration of corticosteroids results in a suppression of the hypothalamo-pituitary-adrenocortical (HPA) axis. The time course of the recovery of the HPA axis depends on the dose and duration of corticosteroid administration. We investigated the recovery of the HPA axis after 14 days of prednisolone administration to rats at a dose of 2.0 mg/rat/day via the drinking water (188 µmol/l). The in vitro corticosterone production by dispersed adrenal cells in response to increasing concentrations of ACTH had recovered 3 days after stopping prednisolone administration. In parallel the initially suppressed plasma corticosterone concentrations had recovered after 3 days, while the pituitary ACTH content had recovered after 5 days. We investigated the possibility to enhance the speed of the recovery of the HPA axis by the simultaneous administration of two drugs with known CRF-stimulating activity via the drinking water. Caffeine in a dose of 100 mg/kg body weight enhanced the recovery of the prednisolone-suppressed HPA axis significantly. One day after the end of prednisolone administration a significant increase in the adrenal weight, in the corticosterone production by dispersed adrenal cells, as well as in the plasma corticosterone concentrations, and in the pituitary ACTH content was observed in the caffeine-treated rats. Chlorimipramine (20 mg/kg body weight), on the other hand, did not influence the prednisolone-mediated suppression of the HPA axis. It is concluded that: (1) simultaneous administration of caffeine enhances the speed of the recovery of the HPA axis after prednisolone administration as evidenced by the full recovery or tendency to recovery of all the investigated components of the HPA axis; (2) chlorimipramine, however, did not influence the suppression of the HPA axis, when administered simultaneously with prednisolone

ISSN:0028-3835    

DOI:10.1159/000125932

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

There is considerable evidence suggesting that endogenous opioids may play an important role in acute stress-induced decreases in luteinizing hormone (LH) release. Studies were undertaken to analyze the role of endogenous opioids in chronic stress-induced decrease in circulating LH and follicle-stimulating hormone (FSH). Chronic restraint (6 h daily over 4 days) evoked a decrease in circulating LH and FSH. Naltrexone treatment, (2 mg/kg three times daily) during the 4 days of restraint, caused an increase in plasma concentrations of LH and FSH, and antagonized the LH suppressory effect of morphine (10 mg/kg) administration. Despite this, naltrexone treatment was ineffective in preventing the inhibitory effect of chronic restraint stress on circulating LH and FSH. Chronic restraint also induced a decrease in hypothalamic LH-releasing hormone (LHRH) content in saline-treated rats. On the contrary, in naltrexone-treated rats, chronic restraint evoked an increase in hypothalamic LHRH content. Thus endogenous opioids and chronic stress seem to act by different mechanisms on the hypothalamic LHRH neuron. In unstressed orchidec-tomized rats, naltrexone administration did not modify circulating LH, but increased plasma concentrations of LH in acutely restrained rats. These data suggest that endogenous opioids may mediate gonadotropin secretion during acute stress, but not during chronic stress.

ISSN:0028-3835    

DOI:10.1159/000125933

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

Quantitative autoradiography was used to evaluate the effects of sex and either 1 or 5 daily 2-hour sessions of restraint stress on binding at 5-HT1A, 5-HT1C and 5-HT2 receptors in the rat dorsal hippocampus. Neither sex nor restraint stress were found to have effects on binding at 5-HT1c or 5-HT2 receptors. However, restraint stress increased binding of [3H]8-hydroxy-2-(di-n-propylamino)tetralin at 5-HT1A receptors in the CA4 region and in the infrapyramidal dentate gyrus. In addition, levels of binding at 5-HT1A receptors in the oriens and lacunosum moleculare layers of the CA1 region were significantly higher in female rats. Neither estradiol benzoate nor estradiol benzoate plus progesterone had effects on binding at hippocampal 5-HTIA receptors in ovariectomized rats, making it unlikely that the sex differences were related to stages of the estrous cycle. Stress-induced levels of corticosterone (CORT) were higher in females. Although CORT levels in blood obtained during restraint decreased from session 1 to session 5 in both male and female rats, the decrease became significant in females only. Female rats also displayed higher levels of activity in the open field. Although activity in the open field was reduced in male and female rats after restraint, these decreases were not significant. Results are discussed in relation to anxiety and depression.

ISSN:0028-3835    

DOI:10.1159/000125951

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

Hormones of the hypothalamo-pituitary-adrenocortical (HPA-) axis are considered to be of physiological and clinical relevance in regulating spontaneous growth hormone (GH) secretion. To further investigate interdependencies between both systems, we studied the effects of adrenocorticotropin [ACTH(1–24)] and human corticotropin-releasing hormone (h-CRH) upon spontaneous GH secretion in 10 male volunteers. Administration of 1 µg ACTH (1–24), 10 µg h-CRH or saline (control: CTL) every hour from 9.00 to 6.00 p.m. resulted in significant differences of cortisol secretion during the entire observation period (8.00 a.m.-3.00 a.m.) between the three groups (p < 0.001, Friedman two-way ANOVA). Mean area under the time course curve (AUC) values (± SEM) for cortisol expressed as ng × 1,000 × min/ml showed also significant differences between the three treatments from 8.00 a.m. to 3.00 a.m.: CTL 64.0 ± 6.4, ACTH(1–24) 178.5 ± 9.4 (p < 0.01, Wilcoxon test), h-CRH 88.5 ± 5.6 (p < 0.01). The main portion of cortisol was released during daytime from 8.00 a.m. to 11.00 p.m., where the most significant differences in the AUC values emerged: CTL 59.6 ± 5.8, ACTH(1–24) 171.5 ± 8.8 (p < 0.01, Wilcoxon test), h-CRH 80.2 ± 5.1 (p < 0.01). With regard to GH secretion, significant differences became obvious between the three treatments during daytime from 8.00 a.m. to 11.00 p.m. and the sleep-related period from 11.00 p.m. to 3.00 a.m. (p < 0.01 and p < 0.02, Friedman two-way ANOVA). The pulse frequency also differed significantly between the treatments during daytime (p < 0.02). Mean AUC values (± SEM) expressed as ng × min/ml for GH from 8.00 a.m. to 11.00 p.m. were: CTL 2,507 ± 614, ACTH(1–24) 3,419 ± 801 (p < 0.02, Wilcoxon test). AUC values for GH from 11.00 p.m. to 3.00 a.m. were: CTL 2,033 ± 368, ACTH(1–24) 1,136 ± 147 (p < 0.02, Wilcoxon test). Also, the number of GH secretory pulses is increased by stimulation with AOΗ(1–24). Stimulation with h-CRH in the same experimental schedule resulted in allusively similar effects, which were less pronounced. While prolonged exposure of somatotrophs to glucocorticoids results in a reduction of GH secretion, short-term exposition to glucocorticoids as resulting from our present stimulation with ACTH(1–24) enhances the amount of GH released. From our current data, we conclude that HPA hormones modulate the spontaneous GH release pattern. This has implications for the interpretation of neuroen-docrine studies in patients with depression, where exaggerated HPA activity often concurs with elevated GH secretion during daytime and decreased GH surges during sleep or

ISSN:0028-3835    

DOI:10.1159/000125937

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

The neurohormone and neurotransmitter somatostatin arises from the processing of a larger precursor, prosomatostatin (proSS). An immunohistochemical investigation in the rat, using a well-characterized antiserum raised against a synthetic peptide identical to the 20–36 residues of the proSS molecule, revealed the presence of immunoreactive nerve fibers and nerve terminals in the median eminence, infundibulum, infundibular stalk and posterior pituitary lobe. The largest number of immunoreactive nerve fibers and nerve terminals was observed in apposition to the portal vessels, whereas a moderate number of proSS-immunoreactive fibers was identified in the infundibular stalk and in the proximal part of the posterior pituitary lobe. The proSS-immunoreactive nerves entered the posterior pituitary lobe from the infundibular and pituitary stalks and were followed to rostral and ventral aspects of the organ. In contrast, positive fibers were rarely identified in caudal and posterior parts. Extracts of rat posterior pituitaries subjected to gel chromatography and reversed-phase high-pressure liquid chromatography (HPLC) analysis showed the presence of a single proSS-immunoreactive molecule corresponding to the size of proSS(l-64). The functional significance of the proSS(l-64) in the hypothalamus and pituitary is at present unknown, but its location in the hypothalamo-hypophy-seal system suggests that this end product of the processing of proSS is released into the portal and perhaps also the general circulatio

ISSN:0028-3835    

DOI:10.1159/000125939

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

The effects of cold exposure on the release of thyrotropin-releasing hormone (TRH) and catecholamines as estimated by push-pull perfusion of the mediobasal hypothalamus were studied. Before cold exposure, the male rats had been kept at room temperature or at 30 °C for 3 weeks. Transfer to 4 °C increased plasma levels of thyroid-stimulating hormone (TSH), but this cold-induced TSH response was more pronounced in animals which had been acclimatized to 30 ° C. Exposure to 4 ° C also increased plasma thyroid hormone levels, but had no effect on plasma prolactin. The hypothalamic content of TRH and dopamine remained similar after transfer to 4 ° C, but after 6 h of cold, the content of noradrenaline and adrenaline had increased 1.6-fold and 3-fold, respectively. In vivo hypothalamic release of TRH, adrenaline and dopamine remained similar during a 2-hour period in control rats kept at room temperature or 30 ° C. The hypothalamic release of TRH, dopamine and adrenaline did not change in rats transferred from room temperature to 4 ° C. The amount of dopamine and adrenaline in push-pull perfusate also remained similar in rats acclimatized to 30 °C after transfer to low temperatures. However, in these rats kept at 30 °C for 3 weeks, exposure to 4 ° C increased TRH release in perfusate from the mediobasal hypothalamus in the first 15 min of cold exposure (2-fold increase). Thus, exposure to cold stimulates the hypothalamo-pituitary-thyroid axis and increases the hypothalamic release of TRH in rats which had been acclimatized to 30

ISSN:0028-3835    

DOI:10.1159/000125940

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

We examined the responses of vasopressin-neurons (VP-neurons) and oxytocin-neurons (OT-neurons) to acute salt-loading in a group of conscious rats (CON, n = 8) and rats under sodium pentobarbital (NEM, 50 mg/kg, i.p., n = 8) or urethane (URE, 1.6 g/kg, i.p. n = 8) anesthesia. Fifteen minutes following the induction of anesthesia, sodium pentobarbital produced an increase in basal plasma osmolality (Posm, 290 ± 2 to 296 ± 3 mosm/kg H2O, p < 0.007) while urethane did not change basal Posm (287 ± 2 to 289 ± 2 mosm/kg H2O). Neither anesthetic agent resulted in any significant changes in basal plasma levels of vasopressin-associated neurophysin (VP-RNP) and oxytocin-associated neurophysin (OT-RNP). In response to intravenous infusion of 18% saline, all three groups of rats had similar rises in Posm. The slopes of the relationship between the rise in plasma VP-RNP and the rise in Posm were markedly reduced in both groups of anesthetized animals compared to that observed for conscious animals (CON = 2.54 ± 0.5; NEM = 1.22 ± 0.18; URE = 1.17 ± 0.24 fmol · mH · mosm–1 · kg H2O–1 p < 0.0126). The slopes of the relationship between the rise in plasma OT-RNP and the rise in Posm were not significantly (p < 0.4478) different between the CON group and the NEM group, while the slope for the URE group was significantly (p < 0.05) smaller than that for the CON group (CON = 10.9 ± 1.5; NEM = 9.3 ± 1.5; URE = 6.3 ± 0.7 fmol · ml–1 · mosm–1 · kg H2O–1). Our data suggest that anesthesia induced by either sodium pentobarbital or urethane significantly reduces the responsiveness of VP-neurons to acute salt loading, but the responsiveness of OT-neurons is lowered by urethane only. It implies that the action of urethane on OT-neurons, and perhaps also on VP-neurons, might be mediated by a mechanism different from that of sodium pentobarbital. Barbiturates are known to reduce the activity at glutamate receptors and also to enhance the activity at γ-aminobutyric acid (GABA) receptors. GABA reportedly is involved in the osmotic release of both OT-neurons and VP-neurons. Therefore, the absence of an effect by pentobarbital on OT-neurons, in addition to its inhibitory influence on VP-neurons, suggests that GABA receptors do not play a predominant role in the actions barbiturates have on the osmotic responsiveness of VP-neurons. Our data might also imply that there is a relative scarcity of glutama

ISSN:0028-3835    

DOI:10.1159/000125941

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

The aim of this study was to elucidate the effects of N-methyl-D-aspartic acid (NMDA) receptor stimulation on the release of several hormones known to be activated during stress. The experiments were performed in conscious freely moving cannulated rats. Systemic administration of N-methyl-D,L-aspartic acid (NMA) and of NMDA in low doses (2.5–10 mg/kg i.p.) was found to induce a dose-related stimulation of adrenocorticotropin (ACTH) release. NMA-induced ACTH release was reduced by administration of an NMDA receptor antagonist (D,L-2-amino-5-phosphonovaleric acid). NMDA was much more potent in activating ACTH release than the racemic form of the amino acid, NMA. In the dose range used, both NMA and NMDA failed to influence prolactin release. With the exception of a small increase in epinephrine concentration in response to the highest dose of NMDA (10 mg/kg), no changes in plasma catecholamines were observed. The data indicate that NMA and NMDA administered in low doses trigger ACTH release without induction of a nonspecific stress respons

ISSN:0028-3835    

DOI:10.1159/000125942

出版商:S. Karger AG    

年代:1991

数据来源: Karger