title: Mechanisms for suckling-induced changes in expression of prolactin receptor in the hypothalamus of the lactating rat.
abstract: The present study aimed to investigate whether increased expression of prolactin receptor (PRL-R) during lactation is caused by suckling-induced hyperprolactinemia or the suckling stimulus itself. Three groups (n=7) of mid-lactating rats were used. Each rat received 3 days of s.c. injection of vehicle or drug before sacrifice on lactation day 10. Rats in the control group received vehicle only and were suckled by pups. The second group received bromocriptine to suppress PRL levels and were suckled by pups. The third group of rats received haloperidol (high PRL) and were deprived of pups. Plasma PRL levels were measured. Animals were perfused with 2% paraformaldehyde for immunofluorescent study. Results showed that PRL-R immunoreactivity in the ventrolateral preoptic, ventromedial preoptic, and ventromedial hypothalamic nuclei was significantly increased in the bromocriptine-treated group compared to the control group, indicating PRL-R expression in these areas may be inhibited by hyperprolactinemia in the presence of the suckling stimulus. The PRL-R in the lateroanterior, ventrolateral and paraventricular nuclei was significantly decreased in the haloperidol-treated group compared to the control group, suggesting that the PRL-R in these areas is most likely regulated by the suckling stimulus itself. The PRL-R in the arcuate nucleus was significantly increased in bromocriptine-treated rats and decreased in haloperidol-treated rats, suggesting that the PRL-R in this nucleus is regulated by mechanisms related to both the stimulus of suckling itself and suckling-induced hyperprolactinemia. These results support the hypothesis that expression of PRL-R in discrete hypothalamic nuclei is differentially regulated by either PRL and/or suckling.
authors.affiliation: Department of Molecular and Integrative Physiology, Kansas University Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66160-7401, USA.
authors.forename: X
authors.initials: X
authors.lastname: Pi
authors.forename: J L
authors.initials: JL
authors.lastname: Voogt
mesh_terms: D000818:Animals; D000833:Animals, Suckling / Q000502:physiology*; D001971:Bromocriptine / Q000494:pharmacology; D018491:Dopamine Agonists / Q000494:pharmacology; D018492:Dopamine Antagonists; D005260:Female; D006220:Haloperidol / Q000494:pharmacology; D006966:Hyperprolactinemia / Q000139:chemically induced / Q000378:metabolism; D007031:Hypothalamus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D007150:Immunohistochemistry; D007774:Lactation / Q000187:drug effects / Q000378:metabolism*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D011388:Prolactin / Q000097:blood* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017448:Receptors, Dopamine D2 / Q000819:agonists / Q000378:metabolism; D011981:Receptors, Prolactin / Q000187:drug effects / Q000378:metabolism*
chemical_list: D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D017448:Receptors, Dopamine D2; D011981:Receptors, Prolactin; D001971:Bromocriptine; D011388:Prolactin; D006220:Haloperidol