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Mechanisms for suckling-induced changes in expression of prolactin receptor in the hypothalamus of the lactating rat.
Brain Res. 2001 Feb 09; 891(1-2):197-205.BR

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+Show Affiliations

Pi X
Department of Molecular and Integrative Physiology, Kansas University Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66160-7401, USA.
Voogt JL
No affiliation info available

MeSH

AnimalsAnimals, SucklingBromocriptineDopamine AgonistsDopamine AntagonistsFemaleHaloperidolHyperprolactinemiaHypothalamusImmunohistochemistryLactationNeuronsProlactinRatsRats, Sprague-DawleyReceptors, Dopamine D2Receptors, Prolactin

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

11164823

Citation

Pi, X, and J L. Voogt. "Mechanisms for Suckling-induced Changes in Expression of Prolactin Receptor in the Hypothalamus of the Lactating Rat." Brain Research, vol. 891, no. 1-2, 2001, pp. 197-205.
Pi X, Voogt JL. Mechanisms for suckling-induced changes in expression of prolactin receptor in the hypothalamus of the lactating rat. Brain Res. 2001;891(1-2):197-205.
Pi, X., & Voogt, J. L. (2001). Mechanisms for suckling-induced changes in expression of prolactin receptor in the hypothalamus of the lactating rat. Brain Research, 891(1-2), 197-205.
Pi X, Voogt JL. Mechanisms for Suckling-induced Changes in Expression of Prolactin Receptor in the Hypothalamus of the Lactating Rat. Brain Res. 2001 Feb 9;891(1-2):197-205. PubMed PMID: 11164823.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mechanisms for suckling-induced changes in expression of prolactin receptor in the hypothalamus of the lactating rat. AU - Pi,X, AU - Voogt,J L, PY - 2001/2/13/pubmed PY - 2001/5/22/medline PY - 2001/2/13/entrez SP - 197 EP - 205 JF - Brain research JO - Brain Res VL - 891 IS - 1-2 N2 - 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. SN - 0006-8993 UR - https://www.unboundmedicine.com/medline/citation/11164823/Mechanisms_for_suckling_induced_changes_in_expression_of_prolactin_receptor_in_the_hypothalamus_of_the_lactating_rat_ DB - PRIME DP - Unbound Medicine ER -