# GONADOTROPIN SECRETION IN VITRO

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA AT DAVIS · 1994 · $213,016

## Abstract

Activation of the luteinizing hormone-releasing hormone (LHRH) receptor by
its agonist triggers multiple signaling pathways and an array of responses.
The immediate event is an explosive exocytosis of LH and involves
postranslational protein modifications.  Delayed responses to LHRH are
manifest within one to several hours and, in some ways, prepare the
gonadotrope for subsequent LHRH challenges.  LHRH self-priming is an
example of a delayed response; it provides for LHRH signal amplification
and as such is a critical component of the preovulatory LH surge.  LHRH
self-potentiation shares strikingly similar characteristics with the
augmentation of LHRH-stimulated LH secretion by either cAMP or acute
progesterone exposure (neither of which can act acutely as a LH
secretagogue).  Our observations have led us to hypothesize that a
signaling pathway stimulated by the LHRH receptor leads to ligand-
independent activation of the progesterone receptor and that this mechanism
is part of the normal, physiological operation of the gonadotrope.  The
goal of the project is the delineation of the LHRH self-priming pathway and
its intersection  with the progesterone receptor.  The specific aims are:
1)  To assess the transcription activation function of the progesterone
receptor in response to stimulation at various points in the post-LHRH
receptor pathway in primary cultured gonadotropes and in a gonadotrope cell
line.  The target of the experimental manipulations will be the PR normally
expressed in the gonadotrope.  2)  To establish a single cell model of
gonadotropin secretion that uses changes in membrane capacitance as a real-
time electrophysiological measure of exocytosis.  This single cell model in
combination with microinjection will be used to define the required role
for cAMP-dependent protein kinase in LHRH self-priming.  Specific targets
will be a PKA pathway and a PKC pathway and their intersection with the PR.
Cell models to achieve these aims will be cultured rat anterior pituitary
cells, gonadotrope-enriched cultures, and a mouse betaT202 clonal
gonadotrope cell line.

## Key facts

- **NIH application ID:** 2196877
- **Project number:** 2R01HD012137-12A1
- **Recipient organization:** UNIVERSITY OF CALIFORNIA AT DAVIS
- **SAM.gov UEI:** TX2DAGQPENZ5
- **Principal Investigator:** JUDITH L TURGEON
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1994
- **Award amount:** $213,016
- **Award type:** 2
- **Project period:** 1979-12-01 → 1996-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/2196877

## Citation

> US National Institutes of Health, RePORTER application 2196877, GONADOTROPIN SECRETION IN VITRO (2R01HD012137-12A1). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/2196877. Licensed CC0.

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