# HYPOTHALAMIC CONTROL OF PROLACTIN

> **NIH NIH R01** · UNIVERSITY OF KANSAS MEDICAL CENTER · 1994 · $168,920

## Abstract

The most common pituitary abnormality is hyperprolactinemia, or the
overproduction and secretion of prolactin (PRL) by lactotroph cells in
the anterior pituitary.  In women this usually results in amenorrhea and
galactorrhea.  Hyperprolactinemia may be the result of macro or
microadenomas of the pituitary, although in many cases the etiology is
not known.  PRL secretion is controlled by numerous factors found in the
hypothalamus, some which act directly on the lactotroph to inhibit or
release PRL, and some which exert their effect on neurons in the
hypothalamus.  The long-term objective is to examine the role of
hypothalamic systems in regulation of PRL during several different
physiological states.  Specific aims are: 1) to examine the catalytic
activity of tyrosine hydroxylase (TH) the initial and rate limiting
enzyme controlling synthesis of DA in TIDA neurons during pregnancy,
lactation, hyper and hypoprolactinemia; 2) to measure TH gene expression
during these states; 3) to determine whether acute changes in TH related
to physiological state are due to alteration in the phosphorylation state
of the TH molecule; 4) to determine the role of calmodulin-dependent and
cAMP dependent kinases in acute TH activation in TIDA neurons, and what
physiological factors regulate this; 5) to establish a long-term TIDA
neuronal culture system in order to assess regulation of TH directly; 6)
to evaluate the regulation of PRL gene expression in the lactotroph.
Neuronal cultures are established in defined media using hypothalamic
tissue of rat fetuses.  Phosphorylation state of TH is determined in
vitro by incorporation of inorganic phosphate into TH.  DA synthesis is
measured by accumulation of L-dihydroxyphenylalanine in the hypothalamus
after addition of a decarboxylase inhibitor.  The relative differences in
mRNA concentration and enzyme quantity for tyrosine hydroxylase is
evaluated by in situ hybridization and immunocytochemistry, respectively.
PRL mRNA levels are determined by dot blot analysis.  Elevated levels of
PRL or placental lactogen-I (PL-I) in the rat is accomplished by
injection of tumor cells that specifically secrete PRL (MMQ) or PL-1
(Rcho) into rats or by infusing PL-I itself.  Dispersed pituitary cells
are used in culture to assess the effect of PL and PRL feedback on
responsiveness of lactotrophs to prolactin releasing factors.  Hormone
levels are determined by radioimmunoassays.  Monoamines are measured by
HPLC.

## Key facts

- **NIH application ID:** 2199076
- **Project number:** 5R01HD024190-06
- **Recipient organization:** UNIVERSITY OF KANSAS MEDICAL CENTER
- **SAM.gov UEI:** YXJGGNC5J269
- **Principal Investigator:** JAMES L VOOGT
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1994
- **Award amount:** $168,920
- **Award type:** 5
- **Project period:** 1988-05-01 → 1997-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/2199076

## Citation

> US National Institutes of Health, RePORTER application 2199076, HYPOTHALAMIC CONTROL OF PROLACTIN (5R01HD024190-06). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/2199076. Licensed CC0.

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