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

Siew H Yip, Nicola Romanò, Papillon Gustafson, David J Hodson, Eloise J Williams, Ilona C Kokay, Agnes O Martin, Patrice Mollard, David R Grattan, Stephen J. Bunn

Research output: Contribution to journalArticlepeer-review

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.
Original languageEnglish
Pages (from-to)1787-1799.E5
Number of pages18
JournalCell Reports
Volume26
Issue number7
Early online date12 Feb 2019
DOIs
Publication statusPublished - 12 Feb 2019

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