# NEURAL AND HORMONAL REGULATION OF LACTATION

> **NIH NIH R01** · PENNSYLVANIA STATE UNIVERSITY, THE · 1994 · $156,456

## Abstract

When lactating rats are injected with the dopamine (DA) agonist
bromocriptine during days 2-5 postpartum, which substantially
decreases the concentrations of PRL in mild without abolishing
lactation, their offspring exhibit decreased activity of the
tuberoinfundibular DA (TIDA) system and elevated serum PRL as young
adults.  In addition, in the adult, there are more cells in the
pituitary glands for neonatal PRL-deficient rats, and their
lactotrophe cells show decreased responsiveness to the PRL-
inhibiting effects of DA and increased responsiveness to the PRL-
stimulating effects of TRH.  These effects 1) are not due to non-
specific effects of bromocriptine since essentially undetectable
levels of the drug pass from the mother to the neonate via the
milk; 2) are prevented by the replacement of PRL to bromocriptine
treated mothers; and 3) do not occur if bromocriptine is
administered to the mothers during the second postnatal week.
These findings suggest the hypothesis that milk-derived PRL in the
neonate influences the growth and/or maturation of TIDA neurons as
well as pituitary lactotrophes, and that a deficiency in mile-
derived PRL during a critical postnatal period may have long-
lasting consequences for neuroendocrine regulation of PRL
secretion.  The specific aims of the present proposal are:  1) to
establish the normal time course for the functional development of
the TIDA system, using measurements of DA concentration and
synthesis rate, and to test the effects of PRL ad of neonatal PRL
deficiency on the course of this development; 2) to investigate the
effects of neonatal PRL deficiency on the numbers of TIDA neurons,
using immunocytochemistry for tyrosine hydroxylase; 3) to examine
whether neonatal PRL deficiency alters the response of TIDA neurons
to their normal regulatory influences, using in vivo and in vitro
approaches; 4) to investigate the consequences of neonatal PRL
deficiency on the adult regulation of PRL synthesis and release by
stimulatory or inhibitory hypophyseotropic hormones, or by
estradiol, using cultured anterior pituitary cells; 5) to test
whether the receptor binding of hypophyseotropic hormones and/or
their coupling to a second messenger system, such as adenylate
cyclase/cAMP, are permanently altered by neonatal PRL deficiency;
6) to test whether neonatal PRL deficiency affects the numbers
and/or morphology of pituitary lactotrophe cells, the secretory
forms of PRL, and the characteristics of PRL secretion from
lactotrophe cells over the lifespan of the rat.

## Key facts

- **NIH application ID:** 2194844
- **Project number:** 3R01HD004358-33S1
- **Recipient organization:** PENNSYLVANIA STATE UNIVERSITY, THE
- **SAM.gov UEI:** NPM2J7MSCF61
- **Principal Investigator:** CRAIG R BAUMRUCKER
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1994
- **Award amount:** $156,456
- **Award type:** 3
- **Project period:** 1977-09-30 → 1995-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/2194844

## Citation

> US National Institutes of Health, RePORTER application 2194844, NEURAL AND HORMONAL REGULATION OF LACTATION (3R01HD004358-33S1). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/2194844. Licensed CC0.

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