摘要:

The concentration of corticotropin-releasing factor (CRF)-binding sites decreases in the rat anterior pituitary after adrenalectomy; this change may be related either to a direct effect of the circulating glucocorticoids at the pituitary level or to a desensitization of CRF receptors through an increased CRF release in hypophysial portal blood. In order to examine the latter possibility we have measured plasma adrenocorticotropin hormone (ACTH) levels and the number of anterior pituitary CRF binding sites in sham-operated and 24-hour adrenalectomized rats after blockade of endogenous CRF by passive immunization with an antiserum anti-rat CRF (CRF-AS), or after injection of normal rabbit serum (NRS). In NRS-injected rats, after sham operation, plasma ACTH concentration increased (227 + 34 vs. 118 ± 19 pg/ml in controls) without change in CRF-binding sites capacity (20.7 ± 2.6 vs. 24.6 ± 3.5 fmol/mg protein in controls). Adrenalectomy induced a large rise in plasma ACTH (785 ± 89 pg/ml) and a decrease in the number of CRF-binding sites (12.2 ± 1.7 fmol/mg protein). After CRF-AS injection, plasma ACTH was normalized in sham-operated animals (149 ± 24 pg/ml) and significantly reduced in adrenalectomized rats (472 ± 76 pg/ml); the adrenalectomy-induced decrease in the number of CRF-binding sites was unaffected by the CRF-AS administration (12.2 ± 1.7 fmol/mg protein). The administration of dexamethasone to adrenalectomized rats significantly reduced plasma ACTH concentrations (23.3 ± 10.6 pg/ml) and prevented the loss in CRF-binding sites capacity (20.7 + 1.3 fmol/mg protein). Affinity of CRF for its binding sites was unchanged in all the groups studied. These findings suggest that the postadrenalectomy reduction in the number of anterior pituitary CRF-binding sites may be mainly due to a direct glucocorticoid effect at the pituitary level rather than a consequence of a possible increased CRF s

ISSN:0028-3835    

DOI:10.1159/000124780

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Behavioral experiments tested the idea that the substance P (SP) innervation of the midbrain central gray (MCG) may be involved in the hormonal induction of sexual receptivity in female rats. SP, a SP antiserum or a reported SP antagonist were injected bilaterally into the MCG in ovariectomized, estrogen-treated females, and the lordosis response was recorded at repeated intervals. In the first experiment, three doses of SP (50, 500 and 1,000 ng/cannula), a single dose of LHRH (50 ng/cannula) or vehicle were given to separate groups of females. All three doses of SP produced a rapid and long-lasting (3 h) increase in lordosis scores in moderately receptive females in tests with either manual stimulation or male rats. This facilitation was similar in latency, magnitude and duration to that produced by LHRH. In the second experiment, the basic findings of experiment 1 were replicated using blind testing. As no dose-response relation was established in experiment 1, a lower dose of SP (10 ng/cannula) was used in addition to doses of 50 and 500 ng/cannula also used in experiment 1. All three doses produced similar long-lasting increases in lordosis scores as in experiment 1. MCG injections of SP also increased lordosis scores in a second series of tests using manual stimulation alone. This demonstrates that the SP-induced facilitation does not depend on an interaction between the injections and stimuli delivered only by the male rat, eg., vaginal stimuli or ultrasonic calls. The question of the importance of endogenous SP for receptivity was examined in experiment 2 using MCG injections of a SP antiserum or the SP analogue, (D-Pro2, D-Trp7,9)-SP, which has been reported to block the excitation of locus coeruleus neurons by SP. The antiserum significantly reduced the group lordosis scores, while the putative antagonist did not. In conclusion, our data support the idea that the SP neurons which innervate the MCG form part of the circuitry controlling the lordosis response.

ISSN:0028-3835    

DOI:10.1159/000124781

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

The possibility that neuropeptide Y (NPY) exerts organizational effects on central noradrenergic systems was investigated by treating newborn rats with subcutaneous injections of a specific NPY-antiserum. Three months later, neuroendocrine function was determined by measuring plasma vasopressin following haemorrhage, since this response is known to be regulated by ascending noradrenergic pathways. Basal mean arterial pressure, heart rate and plasma vasopressin were similar in both control (normal rabbit serum-treated) and NPY-antiserum-treated rats. Treatment with this antiserum resulted in an impaired vasopressin response to haemorrhage, although the haemodynamic changes observed after this hypovolaemic challenge were similar to control rats. NPY and noradrenaline content in the hypothalamus and brainstem were examined at the end of these experiments. NPY-like immunoreactivity was similar in both groups of animals. However, electrochemical detection of noradrenaline after HPLC revealed significantly higher levels in the hypothalamus, but not brainstem, of NPY-antiserum-treated rats. The presence of enduring changes in noradrenaline levels and neurohypophyseal function following neonatal treatment with NPY-antiserum suggests a role for NPY in postnatal organization of the rat hypothalamus.

ISSN:0028-3835    

DOI:10.1159/000124782

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

An episodic secretion of LHRH in pituitary portal blood was observed in ovariectomized and hypophysectomized rats under Saffan anesthesia. This anesthetic did not effect the pulsatile release of LH in ovariectomized rats. Third-ventricular administration of an LHRH agonist, at a concentration which did not cross-react in the LHRH RIA, suppressed both the pulse amplitude and frequency of LHRH release. This inhibitory action of the LHRH agonist on LHRH release was blocked by an LHRH antagonist.

ISSN:0028-3835    

DOI:10.1159/000124783

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

To determine whether the plasma membrane is a primary site for progesterone (P4) action on the neural LHRH apparatus of hypothalamic tissues derived from ovariectomized, estradiol-primed (OVX + E2) immature rats, immobilized P4 was infused directly to these tissues using a superfusion technique. Two kinds of immobilized P4 with bovine serum albumin (BSA) conjugated at positions 3 or 11, or 11-deoxycorticosterone (DOC) immobilized at position 21 of the steroid molecule, respectively, were tested for structural specificity. Among the three immobilized steroids, only P4 with BSA conjugated at position 3 (P4–3-BSA) was effective in stimulating LHRH release in vitro. P4-3-BSA at 0.5 µg/ml, approximately 1.7 × 10–7M of P4, increased LHRH levels in the superfusates to about 2.5-fold those of pretreatment levels. In addition, no conversion of P4–3-BSA to free progesterone was detected. This observation demonstrated that the plasma membrane is a primary site for the stimulating effect of P4 on LHRH release from hypothalamic tissue i

ISSN:0028-3835    

DOI:10.1159/000124784

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

An antiserum (ARK-1) specific to the gonadotropin-releasing hormone precursor (proGnRH) was produced by immunizing with a synthetic peptide (proGnRH 6–16; Gly-Leu-Arg-Pro-Gly-Gly-Lys-Arg-Asp-Ala-Glu) which bridges the proteolytic cleavage site of proGnRH. When used in the radioimmunoassay, ARK-1 bound 25% of the iodinated 5–16 fragment at a 1:30,000 dilution with a sensitivity of 1 pg/tube. Using immunohistochemical techniques, we observed that in serial and the same sections through the preoptic-basal hypothalamus (POA-BH), the precursor molecule was primarily present in the cell soma, whereas GnRH was found in the cell soma, nerve fibers, and terminals of the same neurons. These data indicate that the processing of proGnRH to biologically active peptides (e.g., GnRH) in the rhesus macaque and the baboon POA-BH primarily occurs in the cell s

ISSN:0028-3835    

DOI:10.1159/000124785

出版商:S. Karger AG    

年代:1987

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000124786

出版商:S. Karger AG    

年代:1987

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000124787

出版商:S. Karger AG    

年代:1987

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000124770

出版商:S. Karger AG    

年代:1987

数据来源: Karger