摘要:

We have previously shown that, as seen in the adult rat, pituitary LHRH receptor content declines during the hours encompassing the first preovulatory LH surge. This decrease in receptor number was prevented, however, when pituitary membranes were treated with MgCb to dissociate endogenously bound ligand(s). The present study investigates: (a) whether the first proestrous reduction in available LHRH receptors can be reversed by subjecting the pituitary membranes to a less drastic, dilution-washing procedure previously reported to be highly effective in dissociating bound LHRH, and (b) whether Nembutal blockade of the proestrous decline in LHRH receptors also prevents the dissociation-induced exposure of additional LHRH binding sites. A premature LH surge was induced by exposing juvenile female rats to proestrous-type levels of plasma estradiol (E2) via Silastic capsules. A decline in available LHRH receptors was found around the time of this steroid-induced LH surge. A marked increase in receptor number was, however, observed upon dilution-washing of the membranes. The increase in receptor number was not accompanied by any changes in receptor affinity (Ka). Nembutal administration blocked both the LH surge and the decline in available LHRH receptors. Moreover, dilution-washing of pituitary membranes from Nembutal-treated rats failed to uncover additional LHRH binding sites. The results suggest that a significant portion of the proestrous decline in pituitary LHRH receptors is due to a reduced availability of the receptor to binding. Whether such a phenomenon is due to true occupancy by endogenous ligand(s) or to binding-dependent localization of the receptor within the cell membrane is unclear. Nevertheless, the capacity of Nembutal to prevent both the proestrous decline in receptor number and the exposure of unavailable binding sites indicates that increased release of LHRH and/or LHRH-like molecules is necessary for the sequestration of LHRH binding sites into a nonavailable, membrane-located pool during the afternoon of proestrus.

ISSN:0028-3835    

DOI:10.1159/000124184

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The object of this study was to determine the influence of ovarian steroids on pulsatile LH release in the interval between the mornings of diestrus 2 (D2) and proestrus in the rat. Four groups of rats were bled continuously for 3 h between 09.30–12.30 h at a rate of 75 µl whole blood/6 min: (1) bled on D2; (2) sham ovariectomy (OVX) on D2 and bled on proestrus; (3) OVX on D2, implanted with empty or oil-filled capsules, and bled 24 h later; and (4) OVX on D2, implanted with estradiol (E2) capsules, and bled 24 h later. Between D2 and proestrus, plasma E2 levels increased from 13 ± 1 to 42 ± 9 pg/ml, and progesterone levels decreased from 27 ± 3 to 13 ± 2 ng/ml, the latter reflecting the decline of the corpus luteum early on D2. Between D2 and proestrus there was no change in mean blood LH levels, LH pulse amplitude, or pulse frequency. However OVX on D2 increased mean blood LH levels 2.5-fold over values on proestrus due to a 3.5-fold elevation in LH pulse amplitude and an 80% increase in pulse frequency. E2 levels fell in these rats to 8 ± 1 pg/ml. Restoration of physiological proestrous levels of E2 (46 ± 5 pg/ml) significantly reduced the increase in mean blood LH levels by lowering pulse frequency to proestrous values, and by causing a 50% reduction in pulse amplitude. However, LH pulse amplitude and therefore mean blood LH levels were still higher than values on proestrus. The possibility that ovarian progesterone might also regulate LH pulse amplitude in the D2-proestrous interval was ruled out since there were no significant differences in plasma progesterone levels between 13.00–19.00 h following sham OVX or OVX of rats earlier on the morning of D2. In vitro incubation studies with anterior pituitaries from rats ovariectomized 24 h prior on D2 and implanted with E2 or empty capsules demonstrated that E2 increased the pituitary sensitivity to LHRH, indicating that the E2-induced decrease in LH pulse amplitude could not be exerted at the pituitary level. In conclusion, since LH pulse amplitude and frequency remain unchanged between the mornings of D2 and proestrus, yet increase following OVX, the present data demonstrate that ovarian E2 acts centrally to exert a restraining effect on both parameters of pulsatile LH secretion during this interval in the rat est

ISSN:0028-3835    

DOI:10.1159/000124185

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The electrophysiological properties of gonadotrophs have been studied in vitro, using the ovine adenohypophyseal pars tuberalis as a naturally enriched source of this cell type. Trypsin-dispersed pars tuberalis cells maintained in primary tissue culture had a membrane potential of -72 ± 4 mV (mean ± SEM) and an input resistance of 314 ± 38 MΩ. Spontaneous action potentials were not observed; however, a single spike could be induced by depolarizing current injection. The hypophysiotrophic peptide gonadotrophin-releasing hormone (GnRH) increased membrane voltage fluctuations, but these fluctuations (± 5–10 mV) did not induce action potentials or changes in membrane potential or resistance. Power spectra obtained from analysis of this noise indicated that the fundamental event underlying GnRH action has a mean life-time of 38.4 ± 4.5 ms. The obervations that cells incubated in recording medium secreted luteinizing hormone in response to GnRH and that the GnRH-induced increase in voltage noise was inhibited by Ca2+ channel antagonists support the hypotheses (1) that gonadotrophin secretion is initiated by GnRH-induced Ca2+ channel activation and (2) that action potentials are not a prerequisite for gonadotrophin

ISSN:0028-3835    

DOI:10.1159/000124186

出版商:S. Karger AG    

年代:1985

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000124187

出版商:S. Karger AG    

年代:1985

数据来源: Karger