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Hypothalamic control of prolactin secretion during the perinatal period in the rat
Insights
Hypothalamic control of prolactin (PRL) secretion develops during rat gestation. Pituitary sensitivity to dopamine decreases while sensitivity to thyrotropin-releasing hormone (TRH) increases, influencing PRL levels.
Area of Science:
- Endocrinology
- Neuroscience
- Developmental Biology
Background:
- Hypothalamic regulation of prolactin (PRL) secretion is crucial for mammalian reproduction and development.
- Understanding the developmental trajectory of PRL control is essential for identifying potential disruptions.
Purpose of the Study:
- To investigate the development of hypothalamic control over PRL secretion in rats during late prenatal and early postnatal periods.
- To characterize the roles of thyrotropin-releasing hormone (TRH) and dopamine in modulating PRL secretion during development.
Main Methods:
- Static incubation system for rat pituitaries from fetal day 18 to postnatal day 8.
- Measurement of PRL in incubation medium and pituitary content.
- Coincubation of pituitaries with hypothalamic and cerebral cortical extracts.
- In vitro stimulation with TRH and dopamine agonist apomorphine.
- Immunoneutralization of hypothalamic TRH.
Main Results:
- PRL secretion detected from fetal pituitaries as early as day 18, increasing significantly between days 20-21 prenatally.
- Hypothalamic extracts stimulated PRL secretion in fetuses and neonates, while adult hypothalamic extracts stimulated neonatal pituitaries.
- TRH stimulated PRL secretion in fetal pituitaries, with diminished response postnatally.
- Apomorphine inhibited PRL secretion, with increasing sensitivity with age.
- High PRL release and relative pituitary insensitivity to dopamine contribute to high neonatal PRL levels.
Conclusions:
- Hypothalamic regulation of PRL secretion undergoes significant development during late gestation and early postnatal life.
- Both stimulatory (e.g., TRH) and inhibitory (e.g., dopamine) factors contribute to dynamic PRL secretion patterns.
- Developmental changes in pituitary sensitivity to hypothalamic factors are key to establishing mature PRL regulation.
Abstract:
The development of hypothalamic control of PRL secretion in the late prenatal and early postnatal periods in the rat was studied by employing a static system for incubation of pituitaries. PRL was detected in the incubation medium after incubating fetal pituitaries as early as day 18. A gradual increase in the amount of hormone released into the medium occurred during development, with the greatest change occurring between days 20 and 21 prenatally. A progressive increase in the pituitary content of PRL occurred during development. The percentage of PRL released from the gland was higher pre- (19-39%) than postnatally (17%). Hypothalamic extracts from fetuses and neonates stimulated the secretion of PRL when coincubated with pituitaries from animals of the same age. However, extracts from 1-day-old neonates inhibited PRL secretion from adult male hemipituitaries. Extracts prepared from adult male hypothalami stimulated PRL secretion from neonatal pituitaries from rats at 1 day of age, as did cerebral cortical extracts from adults, but not 1-day-old, rats. TRH significantly stimulated PRL secretion in vitro from pituitaries of donors as early as day 19 of the fetal period. The response of the pituitaries to this peptide diminished by day 8 postnatally. Immunoneutralization of hypothalamic TRH significantly decreased but did not abolish the PRL-releasing activity of hypothalamic extracts, whereas this procedure had no effect on the GH-releasing activity of the extracts. The dopamine receptor agonist apomorphine (10(-5) M) inhibited PRL secretion in vitro on day 19 of the fetal period and postnatally starting on day 1. The response to apomorphine increased with advancing age. The results suggest that a combination of factors contribute to maintaining high circulating PRL levels during the late fetal and early neonatal periods. These include high rates of PRL release by the pituitary and a relative insensitivity of the pituitary to dopamine in the face of high sensitivity to PRL-releasing factors such as TRH.