# BRAIN MONOAMINES AND LUTEINIZING HORMONE SECRETION

> **NIH NIH R01** · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · 1994 · $150,024

## Abstract

The overall objective of this research project is to investigate the
neurochemical mechanisms by which the ovarian hormones, estradiol (E2) and
progesterone (P), exert their feedback controls over the secretion of
luteinizing hormone (LH) from the anterior pituitary gland, and the overall
hypothesis under investigations that the stimulatory and inhibitory effects
of the ovarian hormones on the secretion of LH are mediated by changes in
the activity of monoaminergic and peptidergic systems that regulate,
directly or indirectly, the neurosecretion of LH-releasing hormone (LHRH)
from the median eminence.  This renewal application focusses on the
interplay between the adrenergic neurotransmitters, norepinephrine (NE)
and epinephrine (EPI), and neuropeptides, including endogenous opioids and
neuropeptide Y, in mediating aspects of ovarian hormone positive feedback
on LHRH and LH secretion in adult female rats, and secondly, on the effects
exerted by gonadal hormones during the early neonatal period that influence
the responsiveness of these neurotransmitter and neuropeptide systems to
ovarian hormones in adulthood.  The specific aims of this proposal are
first, to further investigate the interactions between the adrenergic
neurotransmitters and NPY and between NPY and LHRH in mediating ovarian
hormone positive feedback.  These experiments will examine the involvement
of adrenergic and NPY systems in inducing the changes in LHRH
concentrations in the median eminence that precede the ovarian hormone-
induced LH surge and in mediating the stimulatory effect of P on LHRH
release in vitro.  Additional studies will investigate the action of opioid
and GABA systems to regulate NPY and adrenergic transmission controlling
LHRH release, and will further characterize the mechanisms and the
physiological significance of the facilitation by NPY of LHRH-induced LH
release from anterior pituitary cells.  The second specific aim is to
examine whether ovarian hormones, and adrenergic, opioid and/or GABA
systems influence the levels of NPY precursor mRNA in the medial basal
hypothalamus.  The third set of studies will more completely characterize
the changes in adrenergic-peptidergic control over LHRH neurosecretion in
rats defeminized by early exposure to E2, specifically by testing whether
the neurochemical antecedents of the LH surge induced in normal females by
ovarian hormones or antagonists at opioid or GABA receptors (i.e.,
accumulation of LHRH and NPY, activation of NE/EPI turnover) occur in
feminized animals, but fail to occur in defeminized animals, of both sexes.

The fourth specific aim is to investigate whether defeminization by
neonatal exposure to E2 affects the development of the inhibitory EOP and
GABAergic controls over the release of adrenergic transmitters and LHRH,
and whether neonatal exposure to E2 with respect to ovarian hormone
positive feedback mechanisms.

## Key facts

- **NIH application ID:** 2197024
- **Project number:** 5R01HD013703-15
- **Recipient organization:** UNIVERSITY OF TENNESSEE HEALTH SCI CTR
- **SAM.gov UEI:** X1M1PN3KG3E7
- **Principal Investigator:** WILLIAM R CROWLEY
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1994
- **Award amount:** $150,024
- **Award type:** 5
- **Project period:** 1979-12-01 → 1995-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/2197024

## Citation

> US National Institutes of Health, RePORTER application 2197024, BRAIN MONOAMINES AND LUTEINIZING HORMONE SECRETION (5R01HD013703-15). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/2197024. Licensed CC0.

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