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Prolactin

About: Prolactin is a research topic. Over the lifetime, 22356 publications have been published within this topic receiving 609537 citations. The topic is also known as: lactotropin, & PRL,.


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Journal ArticleDOI
TL;DR: Data support the concept that greater responsiveness and sensitivity to PRL during transition to lactation may be associated with an increase in subsequent milk yield.

139 citations

Journal ArticleDOI
TL;DR: The present study suggests that only serotonergic drugs produce similar effects on release of prolactin and TSH, whereas drugs that alter CA and pilocarpine depress prolact in release but have little or no effect of TSH.
Abstract: The effects of a single injection of drugs on serum prolactin and TSH were determinedin male and in estrogen-primed ovariectomized rats. The precursor of serotonin, 5-hydroxytryptophan (5-HTP), produced a significant rise in serum prolactin and TSH, whereas para chloroamphetamine,a depletor of serotonin, elicited a fall in serum prolactin and TSH. α-methylmetatyrosine (α-MMT) and reserpine, both depressors of brain catecholamine (CA) and serotonin levels, evoked significant increases in serum prolactin and reductions in serum TSH. Injection of α-MMT or reserpine together with 5-HTP further elevated serum prolactin but prevented any significant change in serum TSH. This suggests that the ability of α-MMT and reserpine to inhibit TSH release is mediated through a reduction in brain serotonin and not via a decrease in CA. α-methylparatyrosine, which inhibits CA synthesis without altering serotonin, evoked a marked increase in serum prolactin but had no effect on serum TSH. L-dopa administration significantly...

139 citations

Journal ArticleDOI
TL;DR: The finding of testosterone stimulation of brain PRL message and undetectable levels of Pit-1 (GHF-1) in hypothalamic and extrahypothalamic brain regions indicates that the transcriptional regulation of PRL in the brain is different from that in the anterior pituitary.
Abstract: Previous work by our laboratory has described the presence and widespread distribution of a PRL-like immunoreactive protein in brain. The persistence of this PRL in brain after hypophysectomy provided substantial evidence that brain PRL represented the product of a synthetic pool separate from that of the anterior pituitary PRL. To pursue this concept of independent synthesis further, we sought to determine whether brain tissue expressed PRL mRNA. Although we were easily able to detect a single species of PRL mRNA in pituitary by Northern hybridization, we could not visualize message in hypothalamus or extrahypothalamic brain by this technique. Therefore, we performed the polymerase chain reaction on cDNAs from anterior pituitary, hypothalamus, discrete extrahypothalamic brain regions, and other tissues. Hypothalamus and extrahypothalamic brain parts, including the cerebellum, caudate, brain stem, amygdala, thalamus, cortex, and hippocampus, were all positive to varying degrees. Lung and liver were negative, and anterior pituitary was consistently positive. All positive tissues, including anterior pituitary, expressed two hybridization signals: the expected amplified product and another smaller one. The smaller amplified product is presumably the result of an alternatively spliced transcript that is missing part of the PRL gene. Hypophysectomized animals did not express PRL message in brain, but expression was restored in hypophysectomized animals treated with testosterone. Transcripts for Pit-1 (GHF-1), a transcription factor important in regulation of pituitary PRL, were not detected in hypothalamus or any of the extrahypothalamic brain parts. The finding of testosterone stimulation of brain PRL message and undetectable levels of Pit-1 (GHF-1) in hypothalamic and extrahypothalamic brain regions indicates that the transcriptional regulation of PRL in the brain is different from that in the anterior pituitary.

139 citations

Book ChapterDOI
TL;DR: This chapter describes the concept of the hormone—Inhibin, which has an effect on gonadal function in males and females by a reduction of FSH secretion, but a direct action on the gonad also is suspected.
Abstract: Publisher Summary This chapter describes the concept of the hormone—Inhibin. This hormone is formed in the seminiferous tubules by Sertoli cells in males and by granulosa cells in the follicles of females. Inhibin is peptidic in nature. Its biological action is destroyed by digestion with trypsin or pepsin and by heat. It induces antibodies capable of neutralizing endogenous inhibin in adult male or female animals into which they are injected. Inhibin exerts preferential inhibition on the synthesis and release of follicle-stimulating hormone (FSH) by pituitary gonadotrophs maintained in culture. The dose requires to exert an effect on luteinizing hormone (LH) is much higher. It reduces the amount of endogenous LH-releasing hormone (RH) in the hypothalamus maintained in culture. In the intact animals, the observed effect on gonadotropin levels is the result of the action of inhibin at both sites. Inhibin has no effect on the secretion of thyroid-stimulating hormone (TSH), prolactin, or growth hormone either in vivo or in vitro . It also has an effect on gonadal function in males and females by a reduction of FSH secretion, but a direct action on the gonad also is suspected.

139 citations

Journal ArticleDOI
TL;DR: Initiation of the rapid phase of testicular growth at 25 days could be correlated with the elevations of serum FSH and prolactin levels, and rapid growth of sex accessories began somewhat later in the presence of continued relatively high prol actin levels and falling levels of FSH.
Abstract: Serum levels of FSH, LH and prolactin were determined during development in male rats. Blood was collected from the trunk after decapitation. Prolactin levels were very low at 15 and 20 days of age, underwent an initial rise at 25 days, and then remained relatively constant until 50 days. A secondary increase occurred thereafter to reach maximal adult values at 90 days. Serum FSH was readily detectable at 15 and 20 days, rose to a peak at 25 and 30 days and then declined back to the original levels by 60 days. It remained relatively constant thereafter. On the other hand, serum LH levels underwent a very gradual increase from 15 days to reach a maximum at 70 days which was similar to levels found in adults. Initiation of the rapid phase of testicular growth at 25 days could be correlated with the elevations of serum FSH and prolactin levels. Rapid growth of sex accessories began somewhat later in the presence of continued relatively high prolactin levels and falling levels of FSH. Later growth of the sex ...

139 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023360
2022585
2021202
2020221
2019180
2018172