# EFFECT OF HYPERPROLACTINEMIA IN LH RELEASE

> **NIH NIH R01** · UNIVERSITY OF KENTUCKY · 1993 · $211,706

## Abstract

The longterm objective of this research is to evaluate the neuroendocrine
mechanisms by which hyperprolactinemia (hyperPRL) suppresses female
reproductive function.  The specific aims of this proposal are to test
the working hypothesis that hyperPRL suppresses pulsatile and cyclic LH
release by modulating opiatergic neuronal activity.  We will assess
whether this, in turn, influences the activity of catecholamine-
containing neurons resulting in an altered pattern of GnRH release or
whether opiates directly affect GnRH neurons.  Furthermore, we will test
two corollary hypotheses:  (1) when hyperPRL does not affect LH, it is
because the opiatergic/catecholamine/GnRH link is not functional in that
endocrine milieu; and (b) if we restore the opiatergic/catecholamine/GnRH
pattern, we can restore normal LH secretion, despite the presence of
hyperPRL.  Finally, we will test the hypothesis that hyperPRL compromises
pituitary responsiveness.

To test these hypotheses, we will (1) differentiate the circumstances
under which hyperPRL does and does not suppress LH release; (2) examine
how hyperPRL alters opioid neuronal tone; (3) assess whether hyperPRL-
induced changes in opiate and catecholamine activity determine the
efficacy of hyperPRL to suppress LH; and (4) determine whether hyperPRL
decreases pituitary responsiveness to GnRH.  We will assess opiate tone
using 4 indices of activity:  quantitation of opiate peptide
concentrations in microdissected brain regions, monitoring of patterns of
opiate peptide release into microdialysis probes placed in critical brain
regions, measurement of opiate mRNA expression assessed using in situ
hybridization, and autoradiographic quantitation of opiate receptor
densities in key terminal areas.  Three indices of catecholamine activity
will be autoradiographic quantitation of adrenergic receptor densities.
Patterns of GnRH release will be measured at the pituitary gland using
dialysis methodology.  Pituitary responsiveness will be measured in vivo
and in vitro using the reverse hemolytic plaque assay in combination with
in situ hybridization.

Using this multifaceted approach, we should deepen the understanding of
the neuroendocrine factors that regulate the pulsatile and cyclic release
of LH and how hyperPRL perturbs this balance resulting in a different
pattern of LH secretion.

## Key facts

- **NIH application ID:** 2197255
- **Project number:** 7R01HD015955-11
- **Recipient organization:** UNIVERSITY OF KENTUCKY
- **SAM.gov UEI:** H1HYA8Z1NTM5
- **Principal Investigator:** PHYLLIS M. WISE
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1993
- **Award amount:** $211,706
- **Award type:** 7
- **Project period:** 1982-06-01 → 1995-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/2197255

## Citation

> US National Institutes of Health, RePORTER application 2197255, EFFECT OF HYPERPROLACTINEMIA IN LH RELEASE (7R01HD015955-11). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/2197255. Licensed CC0.

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