Variation in Size of the 'Readily Releasable Pool' of Luteinizing Hormone During the Oestrous Cycle of the Rat

Pickering, A; Fink, George

doi:10.1677/joe.0.0830053

Cited by 63 publications

(21 citation statements)

References 7 publications

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“…The determinants of this heterogeneity are unknown but do not appear to be artifacts of the experimental procedures used to disperse and culture the cells. Cells prepared as described in this paper show maximal secretory responses to GnRH that vary with physiologic state similar to those observed with undissociated fragments of pituitary glands (13)(14)(15). In addition, at maximal GnRH-A concentrations, 15-fold increases in LH secretion over baseline values are observed (Fig.…”

Section: Resultssupporting

confidence: 70%

Simultaneous measurement of hormone release and secretagogue binding by individual pituitary cells.

Smith¹,

Neill²

1987

Proc. Natl. Acad. Sci. U.S.A.

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The quantitative relationship between receptor binding and hormone secretion at the single-cell level was investigated in the present study by combining a reverse hemolytic plaque assay for measurement of luteinizing hormone (LH) secretion from individual pituitary cells with an autoradiographic assay of l251-labeled gonadotropin-releasing hormone (GnRH) agonist binding to the same cells. In the plaque assay, LH secretion induces complement-mediated lysis of the LH-antibody-coated erythrocytes around the gonadotropes, resulting in areas of lysis (plaques). LH release from individual gonadotropes was quantified by comparing radioimmunoassayable LH release to hemolytic area in similarly treated cohort groups of cells; plaque area was linearly related to the amount of LH secreted. Receptor autoradiography was performed using 1251-labeled GnRH-A (a superagonist analog of GnRH) both as the ligand and as the stimulant for LH release in the plaque assay; the developed silver grains appearing over cells in the center of plaques were measured microscopically. The grains appeared to represent specific and high-affinity receptors for GnRH because (t) no pituitary cells other than gonadotropes bound the labeled ligand and (ii) grain development was progressively inhibited by coincubation with increasing doses of unlabeled GnRH-A. Despite high correlations between mean grain number and mean plaque area in doseresponse curves, the correlation coefficients for these parameters were low (range 0.02-0.38) in the individual cells comprising these groups. We conclude that GnRH receptor number for any individual gonadotrope is a weak determinant of the amount of LH it can secrete; nevertheless, full occupancy of all its GnRH receptors is required for any gonadotrope to reach its full LH-secretory capacity. Apparently the levels of other factors comprising the steps along the secretory pathway determine the secretory capacity of an individual cell.The quantitative relationship between receptor binding and hormone secretion has been difficult to establish at the single-cell level because of the presence of "spare receptors" on cells and because of the absence of methods permitting measurement of secretion by individual cells. In the present study, we combined a reverse hemolytic plaque assay for measurement of luteinizing hormone (LH) secretion from individual pituitary cells (1, 2) with an autoradiographic assay of 1251I-labeled gonadotropin-releasing hormone (GnRH) agonist binding to the same cells under conditions in which the spare receptors had been removed by trypsin treatment.The hypothalamic decapeptide GnRH is the key neural regulator of the reproductive process of mammals (3, 4). It is synthesized by hypothalamic neurons and reaches the anterior lobe of the pituitary gland after secretion into the hypothalamohypophyseal portal circulation, the blood vessels comprising a direct link between the hypothalamus and pituitary gland. There, GnRH stimulates the release of LH from the gonadotropes (comprising about 5% of the...

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Section: Resultssupporting

confidence: 70%

Simultaneous measurement of hormone release and secretagogue binding by individual pituitary cells.

Smith¹,

Neill²

1987

Proc. Natl. Acad. Sci. U.S.A.

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“…This migration of secretory granules, shown schematically in Fig. 21, is due presumably to changes in the contractile elements of the cell and may explain in part the increase in the readily releasable pool of LH that occurs before and during the spontaneous ovulatory LH surge (Pickering & Fink, 1979). Since oestrogen enhances the releasing as well as the priming action of LHRH (Fig.…”

Section: Rapid Effects Of Steroidsmentioning

confidence: 99%

The G. W. Harris Lecture Steroid Control of Brain and Pituitary Function

Fink

1988

Exp Physiol

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“…injection of a supramaximal dose of LHRH (1,000 ng/100 g body weight) with that of the LH surge induced by 2 injections of LHRH after oil or proges terone injections ( fig. 1) suggests that in LL rats progester one increases the size of the readily releasable pool of LH [28], Progesterone in the LL rat also increased the magnitude of the priming effect of LHRH (table III, fig-1). Here again the LL rats differed from the LD rats because progesterone given on metestrus did not increase the priming effect of LHRH [2], and in long-term ovariectomized rats primed with E2 the magnitude of the priming effect of LHRH in progesterone-treated rats was not significantly different from that in oil-treated control animals ( fig.…”

Section: Discussionmentioning

confidence: 94%

Effects of Progesterone on the Pituitary Responsiveness to, and Priming Effect of Luteinizing Hormone Releasing Hormone in Female Rats Exposed to Constant Light

Watts¹,

Fink²

1985

Neuroendocrinology

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We have investigated the role of progesterone in the mating-induced release of luteinizing hormone (LH) and ovulation in female rats exposed to a 60-day period of constant light (LL). Plasma LH and progesterone concentrations were increased after mating; plasma estradiol concentrations, although not increased after mating, were increased compared with the concentrations in female rats on light-dark (LD) exposure during diestrus, proestrus evening and estrus. Progesterone induced ovulation in about half the number of female rats exposed to long-term LL, and in these animals, there was a significant increase in pituitary responsiveness to luteinizing hormone releasing hormone (LHRH) 5 h after progesterone injection. The magnitude of the priming effect of LHRH was markedly increased 2 h after progesterone treatment. Treatment with sodium pentobarbitone (SP) 15 min before an injection of progesterone, blocked the increase in pituitary responsiveness to LHRH 5 h later, but treatment with SP 4 h before progesterone injection did not block the increase in the magnitude of the priming effect of LHRH. These results suggest that progesterone acts both at the brain and pituitary to facilitate LH release, and that the increase in plasma progesterone produced by mating is at least partly responsible for the LH surge induced by mating in LL rats.

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Variation in Size of the 'Readily Releasable Pool' of Luteinizing Hormone During the Oestrous Cycle of the Rat

Cited by 63 publications

References 7 publications

Simultaneous measurement of hormone release and secretagogue binding by individual pituitary cells.

Simultaneous measurement of hormone release and secretagogue binding by individual pituitary cells.

The G. W. Harris Lecture Steroid Control of Brain and Pituitary Function

Effects of Progesterone on the Pituitary Responsiveness to, and Priming Effect of Luteinizing Hormone Releasing Hormone in Female Rats Exposed to Constant Light

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