Atlas of the neurons that express mRNA for the long form of the prolactin receptor in the forebrain of the female rat

Bakowska, Joanna C.; Morrell, Joan I.

doi:10.1002/(sici)1096-9861(19970922)386:2<161::aid-cne1>3.0.co;2-#

Cited by 182 publications

(115 citation statements)

References 82 publications

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“…In the present study, approximately twofold increases in longform mRNA were observed, but this change was not statistically significant due to inter-sample variation. Consistent with the present data, Bakowska & Morrell (1997) found no changes in expression of long-form PRL-R mRNA during pregnancy in the ventromedial hypothalamic nuclei. Hence, it seems that changes in mRNA expression are not as pronounced as suggested by our earlier data.…”

Section: Discussionsupporting

confidence: 91%

“…Other studies, using in situ hybridization, have reported subtle changes in levels of long-form PRL-R mRNA (Bakowska & Morrell 1997, Mann & Bridges 2002, but these may well be specific to certain subregions of the nucleus or fluctuate over a relatively short time-course. For example, Mann & Bridges (2002) found the numbers of cells expressing PRL-R mRNA in the medial preoptic nuclei were significantly increased 2 h postpartum, but then declined back to pre-pregnancy levels throughout the remainder of lactation.…”

Section: Discussionmentioning

confidence: 97%

“…Further studies have detected the presence of prolactin-binding sites in the rat brain using in vitro autoradiography (Muccioli et al 1991, Crumeyrolle-Arias et al 1993, Mustafa et al 1994, 1995, and identified PRL-R expression by immunohistochemistry (Roky et al 1996, Pi & Grattan 1998a, 1999a. Similarly, mRNA for PRL-R has been detected in the brain using both RT-PCR (Chiu et al 1992, Sugiyama et al 1994, Pi & Grattan 1998b, 1999b and in situ hybridization (Chiu & Wise 1994, Bakowska & Morrell 1997, Mann & Bridges 2002. Prolactin has been implicated in the regulation of a variety of brain functions, including the suppression of adrenocorticotrophin secretion during the stress response (Torner et al 2001), an increase in feeding and appetite (Sauve & Woodside 1996, 2000, and the suppression of fertility (Cohen-Becker et al 1986), as well as the well-characterized short-loop negative feedback regulation of its own secretion by stimulating tuberoinfundibular dopamine (TIDA) neuronal activity (Freeman et al 2000).…”

Section: Introductionmentioning

confidence: 99%

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Quantitation of prolactin receptor mRNA in the maternal rat brain during pregnancy and lactation

Augustine¹,

Kokay²,

Andrews³

et al. 2003

Journal of Molecular Endocrinology

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Prolactin receptor (PRL-R) expression in the brain is increased in lactating rats compared with non-pregnant animals. The aim of the present study was to determine the time-course of changes in PRL-R mRNA levels during pregnancy and/or lactation, and to determine relative levels of the two forms (short and/or long form) of receptor mRNA in specific brain regions. Brains were collected from female rats on dioestrus, days 7, 14 or 21 of pregnancy, day 7 of lactation or day 7 post-weaning. Frozen, coronal sections were cut (300 µm) and specific hypothalamic nuclei and the choroid plexus were microdissected using a punch technique. Total RNA was extracted and reverse transcribed, then first strand cDNA was amplified using quantitative real-time PCR. Results showed an up-regulation of long-form PRL-R mRNA in the choroid plexus by day 7 of pregnancy compared with dioestrus, which further increased on days 14 and 21 of pregnancy and day 7 of lactation, and then decreased to dioestrous levels on day 7 post-weaning. Short-form PRL-R mRNA levels increased on day 14 of pregnancy relative to dioestrus, increased further on day 7 of lactation and decreased on day 7 post-weaning. Changes in mRNA were reflected in increased levels of PRL-R immunoreactivity in the choroid plexus during pregnancy and lactation, compared with dioestrus. In the arcuate nucleus, long-form PRL-R mRNA was increased during pregnancy. In contrast to earlier work, no significant changes in short-or long-form PRL-R mRNA expression were detected in several other hypothalamic nuclei, suggesting that changes in hypothalamic mRNA levels may not be as marked as previously thought. The up-regulation of PRL-R mRNA and protein expression in the choroid plexus during pregnancy and lactation suggest a possible mechanism whereby increasing levels of peripheral prolactin during pregnancy may have access to the central nervous system. Together with expression of long-form PRL-R mRNA in specific hypothalamic nuclei, these results support a role for prolactin in regulating neuroendocrine and behavioural adaptations in the maternal brain.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Quantitation of prolactin receptor mRNA in the maternal rat brain during pregnancy and lactation

Augustine¹,

Kokay²,

Andrews³

et al. 2003

Journal of Molecular Endocrinology

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“…However, PRL-responsive neurons in specific hypothalamic nuclei and the feedback of PRL on TIDA neurons have been characterized more intensively. This also included the medial preoptic area, the PVN, and limbic structures which are all of specific importance for sexual drive and function (Bakowska & Morrell 1997, Brown et al 2010.…”

Section: Sexual Behavior and Reproductionmentioning

confidence: 99%

Prolactin secretion patterns: basic mechanisms and clinical implications for reproduction

Egli¹,

Leeners²,

Krüger³

2010

Reproduction

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Prolactin (PRL) is one of the most versatile hormones in the mammalian body affecting reproductive, sexual, metabolic, immune, and other functions. It is therefore not surprising that the neural control of PRL secretion is complex, involving the coordinated actions of several hypothalamic nuclei. A plethora of experimental data exists on the hypothalamic control of hormone secretion under various physiological stimuli. There have been even mathematical models and computer studies published, which help to understand the complex hypothalamic-pituitary network. Nevertheless, the putative role of PRL for human reproduction still has to be clarified. Here, we review data on the underlying mechanisms controlling PRL secretion using both experimental and mathematical approaches. These investigations primarily focus on rhythmic secretion in rats during early pregnancy or pseudopregnancy, and they point to the important role of oxytocin as a crucial PRL-releasing factor. Recent data on human studies and their theoretical and clinical implications are reviewed as well. In particular, studies demonstrating a sustained PRL surge after sexual climax in males and females are presented, indicating possible implications for both sexual satiation and reproductive functions. Taking these data together, there is evidence for the hypothesis that the PRL surge induced by sexual activity, together with the altered PRL rhythmic pattern, is important for successful initialization of pregnancy not only in rodents but also possibly in humans. However, further investigations are needed to clarify such a role in humans.

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“…PRL's actions are mediated at the PRL receptor, which is most densely concentrated in the choroid plexus where active uptake of serum PRL occurs. To a lesser degree, the PRL receptor is also distributed in the paraventricular nucleus (PVN) and other hypothalamic sites (Bakowska and Morrell, 1997;Chiu and Wise, 1994;Crumeyrolle-Arias et al, 1993;Walsh et al, 1987) with generally higher densities found in females (Chiu and Wise, 1994;Muccioli et al, 1991;Pi and Grattan, 1998).…”

Section: Prolactin's Physiologic Rolementioning

confidence: 99%

From Galactorrhea to Osteopenia: Rethinking Serotonin–Prolactin Interactions

Emiliano

Fudge

2004

Neuropsychopharmacol

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The widespread use of the selective serotonin reuptake inhibitors (SSRIs) has been accompanied by numerous reports describing a potential association with hyperprolactinemia. Antipsychotics are commonly known to elevate serum prolactin (PRL) through blockade of dopamine receptors in the pituitary. However, there is little awareness of the mechanisms by which SSRIs stimulate PRL release. Hyperprolactinemia may result in overt symptoms such as galactorrhea, which may be accompanied by impaired fertility. Long-term clinical sequelae include decreased bone density and the possibility of an increased risk of breast cancer. Through literature review, we explore the possible pathways involved in serotonin-induced PRL release. While the classic mechanism of antipsychotic-induced hyperprolactinemia directly involves dopamine cells in the tuberoinfundibular pathway, SSRIs may act on this system indirectly through GABAergic neurons. Alternate pathways involve serotonin stimulation of vasoactive intestinal peptide (VIP) and oxytocin (OT) release. We conclude with a comprehensive review of clinical sequelae associated with hyperprolactinemia, and the potential role of SSRIs in this phenomenon.

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Atlas of the neurons that express mRNA for the long form of the prolactin receptor in the forebrain of the female rat

Cited by 182 publications

References 82 publications

Quantitation of prolactin receptor mRNA in the maternal rat brain during pregnancy and lactation

Quantitation of prolactin receptor mRNA in the maternal rat brain during pregnancy and lactation

Prolactin secretion patterns: basic mechanisms and clinical implications for reproduction

From Galactorrhea to Osteopenia: Rethinking Serotonin–Prolactin Interactions

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