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Differential Regulation of Rat Luteinizing Hormone - and β-Subunits During the Stimulatory and Down-Regulatory Phases of Gonadotropin-Releasing Hormone Action^*

Q.X. YUAN, R.S. SWERDLOFF and S. BHASIN

Department of Medicine, Harbor-University of California-Los Angeles Medical Center Torrance, California 9050

Address requests for reprints to: Dr. Shalender Bhasin, Department of Medicine, Division of Endocrinology, Harbor-University of California- Los Angeles Medical Center, 1000 West Carson Street, Torrance, California 90509.

Abstract

Chronic treatment with agonist analogs of GnRH or long term continuous administration of GnRH results in down-regulation of pituitary LH secretion. We investigated the changes in the LH subunits during the stimulatory and down-regulatory phases of GnRH action in rat pituitary cell monolayer culture. The rat pituitary cells in culture, pretreated with medium alone or GnRH agonist for 48 h, were incubated with graded doses of GnRH for 4 h, and LH, LH, and LHβ concentrations in the media and cell pellets were measured by specific and sensitive RIAs. Cells pretreated with medium alone responded to GnRH with a dose-dependent increase in LH, LH, and LHβ immunoreactivity in the medium. However, rat LH, LH, and LHβ concentrations in the cell pellets showed a dose-dependent decrease with GnRH treatment. Pretreatment with GnRH agonist led to a marked decrease in the LH response of cells to graded doses of GnRH. During this down-regulatory phase, the concentrations of LHβ in the medium remained undetectable even though LH immunoreactivity remained persistently and disproportionately elevated. These data suggest that the - and β-subunits of rat LH are both coordinately and differentially regulated. During the stimulatory phase of GnRH action, both subunits rise concordantly, but during the downregulatory phase the secretion of the two subunits becomes unbalanced. The changes in the β-subunit closely parallel the changes in the concentrations of LH dimer, pointing to the key role of β-subunit in regulation of LH secretion. (Endocrinology 122: 504–510, 1988)

Footnotes

^* This work was supported by the New Development Award (to S.B.) of the UCLA Population Research Center and Training Grant 2-T32- AM-07214-03.

Visiting scientist from the Beijing Medical University, Peoples Republic of China, supported by a research training grant from the WHO.

Received December 10, 1986.

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