Elevated prolactin during pregnancy drives a phenotypic switch in mouse hypothalamic dopaminergic neurons

Research output: Contribution to journalArticle

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Elevated prolactin during pregnancy drives a phenotypic switch in mouse hypothalamic dopaminergic neurons. / Yip, Siew; Romano, Nicola; Gustafson, Papillon; Hodson, David; Williams, Eloise; Kokay, Ilona; Martin, Agnes O; Mollard, Patrice; Grattan, David; Bunn, Stephen.

In: Cell Reports, Vol. 26, No. 7, 12.02.2019, p. 1787-1799.

Research output: Contribution to journalArticle

Harvard

Yip, S, Romano, N, Gustafson, P, Hodson, D, Williams, E, Kokay, I, Martin, AO, Mollard, P, Grattan, D & Bunn, S 2019, 'Elevated prolactin during pregnancy drives a phenotypic switch in mouse hypothalamic dopaminergic neurons', Cell Reports, vol. 26, no. 7, pp. 1787-1799. https://doi.org/10.1016/j.celrep.2019.01.067

APA

Yip, S., Romano, N., Gustafson, P., Hodson, D., Williams, E., Kokay, I., Martin, A. O., Mollard, P., Grattan, D., & Bunn, S. (2019). Elevated prolactin during pregnancy drives a phenotypic switch in mouse hypothalamic dopaminergic neurons. Cell Reports, 26(7), 1787-1799. https://doi.org/10.1016/j.celrep.2019.01.067

Vancouver

Author

Yip, Siew ; Romano, Nicola ; Gustafson, Papillon ; Hodson, David ; Williams, Eloise ; Kokay, Ilona ; Martin, Agnes O ; Mollard, Patrice ; Grattan, David ; Bunn, Stephen. / Elevated prolactin during pregnancy drives a phenotypic switch in mouse hypothalamic dopaminergic neurons. In: Cell Reports. 2019 ; Vol. 26, No. 7. pp. 1787-1799.

Bibtex

@article{6248ab6416d547598e5219cdf31ab623,
title = "Elevated prolactin during pregnancy drives a phenotypic switch in mouse hypothalamic dopaminergic neurons",
abstract = "Altered physiological states require neuronal adaptation. In late pregnancy and lactation, a sub-population of the mouse hypothalamic tuberoinfundibular dopaminergic (TIDA) neurons alters their behavior to synthesize and release met-enkephalin rather than dopamine. These neurons normally release dopamine to inhibit prolactin secretion and are activated by prolactin in a short-loop feedback manner. In lactation, dopamine synthesis is suppressed in an opioid-dependent (naloxone-reversible) manner, meaning that prolactin secretion is disinhibited. Conditional deletion of the prolactin receptor in neurons reveals that this change in phenotype appears to be driven by prolactin itself, apparently through an alteration in intracellular signaling downstream of the prolactin receptor that favors enkephalin production instead of dopamine. Thus, prolactin effectively facilitates its own secretion, which is essential for lactation and maternal behavior. These studies provide evidence of a physiologically important, reversible alteration in the behavior of a specific population of hypothalamic neurons in the adult brain.",
keywords = "dopamine, encephalin, hypothalamus, lactation, lactotrophs, neuronal plasticity, prolactin, prolactin receptor, tuberoinfundibular dopaminergic neurons",
author = "Siew Yip and Nicola Romano and Papillon Gustafson and David Hodson and Eloise Williams and Ilona Kokay and Martin, {Agnes O} and Patrice Mollard and David Grattan and Stephen Bunn",
year = "2019",
month = feb
day = "12",
doi = "10.1016/j.celrep.2019.01.067",
language = "English",
volume = "26",
pages = "1787--1799",
journal = "Cell Reports",
issn = "2211-1247",
publisher = "Elsevier",
number = "7",

}

RIS

TY - JOUR

T1 - Elevated prolactin during pregnancy drives a phenotypic switch in mouse hypothalamic dopaminergic neurons

AU - Yip, Siew

AU - Romano, Nicola

AU - Gustafson, Papillon

AU - Hodson, David

AU - Williams, Eloise

AU - Kokay, Ilona

AU - Martin, Agnes O

AU - Mollard, Patrice

AU - Grattan, David

AU - Bunn, Stephen

PY - 2019/2/12

Y1 - 2019/2/12

N2 - Altered physiological states require neuronal adaptation. In late pregnancy and lactation, a sub-population of the mouse hypothalamic tuberoinfundibular dopaminergic (TIDA) neurons alters their behavior to synthesize and release met-enkephalin rather than dopamine. These neurons normally release dopamine to inhibit prolactin secretion and are activated by prolactin in a short-loop feedback manner. In lactation, dopamine synthesis is suppressed in an opioid-dependent (naloxone-reversible) manner, meaning that prolactin secretion is disinhibited. Conditional deletion of the prolactin receptor in neurons reveals that this change in phenotype appears to be driven by prolactin itself, apparently through an alteration in intracellular signaling downstream of the prolactin receptor that favors enkephalin production instead of dopamine. Thus, prolactin effectively facilitates its own secretion, which is essential for lactation and maternal behavior. These studies provide evidence of a physiologically important, reversible alteration in the behavior of a specific population of hypothalamic neurons in the adult brain.

AB - Altered physiological states require neuronal adaptation. In late pregnancy and lactation, a sub-population of the mouse hypothalamic tuberoinfundibular dopaminergic (TIDA) neurons alters their behavior to synthesize and release met-enkephalin rather than dopamine. These neurons normally release dopamine to inhibit prolactin secretion and are activated by prolactin in a short-loop feedback manner. In lactation, dopamine synthesis is suppressed in an opioid-dependent (naloxone-reversible) manner, meaning that prolactin secretion is disinhibited. Conditional deletion of the prolactin receptor in neurons reveals that this change in phenotype appears to be driven by prolactin itself, apparently through an alteration in intracellular signaling downstream of the prolactin receptor that favors enkephalin production instead of dopamine. Thus, prolactin effectively facilitates its own secretion, which is essential for lactation and maternal behavior. These studies provide evidence of a physiologically important, reversible alteration in the behavior of a specific population of hypothalamic neurons in the adult brain.

KW - dopamine

KW - encephalin

KW - hypothalamus

KW - lactation

KW - lactotrophs

KW - neuronal plasticity

KW - prolactin

KW - prolactin receptor

KW - tuberoinfundibular dopaminergic neurons

UR - http://www.scopus.com/inward/record.url?scp=85061097960&partnerID=8YFLogxK

U2 - 10.1016/j.celrep.2019.01.067

DO - 10.1016/j.celrep.2019.01.067

M3 - Article

VL - 26

SP - 1787

EP - 1799

JO - Cell Reports

JF - Cell Reports

SN - 2211-1247

IS - 7

ER -