Estradiol-induced LH release in juvenile female rats: Nembutal blocks both the decline and the exposure of nonavailable pituitary LHRH receptor sites

Sheryl S. Smith, Sergio Ojeda

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

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 MgCh 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 (K.a). 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.

Original languageEnglish (US)
Pages (from-to)246-251
Number of pages6
JournalNeuroendocrinology
Volume41
Issue number3
DOIs
StatePublished - 1985
Externally publishedYes

Fingerprint

LHRH Receptors
Pentobarbital
Gonadotropin-Releasing Hormone
Estradiol
Binding Sites
Membranes
Ligands
Proestrus
Capsules
Steroids
Cell Membrane

Keywords

  • Anterior pituitary gland
  • Estradiol
  • Female puberty
  • LH release
  • LHRH receptors

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Cellular and Molecular Neuroscience
  • Endocrine and Autonomic Systems
  • Neuroscience(all)

Cite this

@article{43bcc35994e54980b474a457d10f9997,
title = "Estradiol-induced LH release in juvenile female rats: Nembutal blocks both the decline and the exposure of nonavailable pituitary LHRH receptor sites",
abstract = "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 MgCh 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 (K.a). 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.",
keywords = "Anterior pituitary gland, Estradiol, Female puberty, LH release, LHRH receptors",
author = "Smith, {Sheryl S.} and Sergio Ojeda",
year = "1985",
doi = "10.1159/000124184",
language = "English (US)",
volume = "41",
pages = "246--251",
journal = "Neuroendocrinology",
issn = "0028-3835",
publisher = "S. Karger AG",
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TY - JOUR

T1 - Estradiol-induced LH release in juvenile female rats

T2 - Nembutal blocks both the decline and the exposure of nonavailable pituitary LHRH receptor sites

AU - Smith, Sheryl S.

AU - Ojeda, Sergio

PY - 1985

Y1 - 1985

N2 - 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 MgCh 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 (K.a). 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.

AB - 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 MgCh 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 (K.a). 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.

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KW - Estradiol

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